Viral Infection of Oral Cavity

Viruses are the smallest known infective agents and are perhaps the simplest form of life known. Viruses do not possess a cellular organization and they do not fall strictly into the category of unicellular microorganisms.

  • Viruses do not have a cellular organization.
  • They contain only one type of nucleic acid, either DNA or RNA but never both.
  • They are obligate intracellular parasites.
  • They lack the enzymes necessary for protein and nucleic acid synthesis and are dependent for replication on the synthetic machinery of host cells.
  • They multiply by a complex process and not by binary fission.
  • They are unaffected by antibacterial antibiotics.
  • Viruses are much smaller than bacteria. The extracellular infectious virus particle is called the virion.
  • Unit for measurement of virion size is nanometers (nm).
  • Viruses vary widely in size from 20 nm to 300 nm.
  • The largest among them is pox virus (300 nm).
  • Smallest viruses are the parvovirus (about 20 nm).
  1. Viral Capsid.
  2. Virus Symmetry.
  3. Viral Envelope.
  4. Viral Nucleic Acids.
  • Viruses consist of nucleic acid core surrounded by a protein coat called capsid.
  • Capsid with the enclosed nucleic acid is known as nucleocapsid.
  • Capsid is composed of a large number of capsomers that form morphological units.
  • The chemical units of capsid (polypeptide molecules) arranged symmetrically to form an impenetrable shell around the nucleic acid core
  • Protects the viral genome from physical destruction and enzymatic inactivation by nucleases in biological material.
  • Provides binding sites forvirus to attach to specific receptor sites on the host cell.
  • Facilitates the assembly and packaging of viral genetic information.
  • Serves as a vehicle of transmission from one host to another.

Viral architecture can be grouped into three types basedon the arrangement of morphologic subunits:

  • Icosahedral symmetry
  • Helical symmetry
  • \Complex structures.
  • Virions may be enveloped or non enveloped (naked).
  • Envelope or outer covering of virus containing lipid is derived from the plasma membrane of the host cell during their release by budding from the cell surface.
  • The envelope is glycoprotein in nature.
  • Viruses contain a single kind of nucleic acid—either DNA or RNA—that encodes the genetic information necessary for replication of the virus.
  • The genome may be single-stranded or double-stranded, circular or linear, and segmented or nonsegmented.
  • In this system viruses are separated into major groupings called families.
  • Virus family names have the suffix –
  • Within each family sub-division called genera.
  • Genus names carry the suffix virus.
  • DNA viruses refer to viruses whose genetic information is stored in the form of DNA.
  • Most DNA viruses are double-stranded viruses, consisting of icosahedral symmetry in their capsid.
  • Few may contain single-stranded DNA in their genome.
  • Some DNA viruses may also contain an envelope.
  • RNA viruses refer to the viruses whose genetic information is stored in the form of RNA.
  • Most RNA viruses contain single-stranded RNA, few contain double-stranded RNA.
  • RNA viruses contain small genomes as compared to DNA viruses. This is due to the error-prone replication in RNA viruses. 
  • Both DNA and RNA viruses can only reproduce inside a living host cell.
  • Most DNA and RNA viruses can be harmful since they infect living cells.
  • Both DNA and RNA viruses contain a capsid.
  • Both DNA and RNA viruses can be either enveloped or non-enveloped.

DNA Viruses

RNA Viruses


DNA viruses refer to viruses whose genetic information is stored in the form of DNA.

RNA viruses refer to viruses whose genetic information is stored in the form of RNA.



DNA viruses contain DNA as their genetic material.

RNA viruses contain RNA as their genetic material.



Double-stranded DNA viruses are more common than single-stranded DNA viruses.

Single-stranded RNA viruses are more common than double-stranded RNA viruses.




Viral DNA is replicated inside the nucleus of the host cell.

Viral RNA is first transcribed and then is replicated in the cytoplasm.

Protein Synthesis

Viral DNA is first transcribed into RNA, and then mRNA is translated into viral proteins.

RNA viruses can bypass transcription during protein synthesis since they already contain RNA in the genome.


DNA viruses are stable due to the lower mutation rate.

RNA viruses are unstable due to the higher mutation rate.

Fidelity of Replication


DNA viruses show an accurate replication.

RNA viruses show an error-prone replication.

Size of the Genome


DNA viruses contain a large genome.

RNA viruses contain a small genome.



Newly-synthesized viral DNA is packed into a pre-formed capsid called procapsid.

Newly-synthesized viral RNA should be protected from degradation since a procapsid is not formed in RNA viruses.



Class I, II, and VII of the Baltimore classification of viruses are DNA viruses.

Class III, IV, V, and VI of the Baltimore classification of viruses are RNA viruses.



Adenoviruses, Herpesviruses, Poxviruses, Parvoviruses, and Hepadnaviruses 

Reoviruses,  Picornaviruses, Togaviruses,

Orthomyxoviruses, Rhabdoviruses,  and Retroviruses

Associated Diseases


Smallpox, herpes, and chickenpox

Aids, Ebola hemorrhagic fever, SARS, the common cold, influenza, hepatitis C, West Nile fever, polio, and measles

  • The human herpesviruses are large (typically 100-200 nm), enveloped (i.e. membrane-bound) viruses.
  • They contain double-stranded DNA genomes packed in an icosahedral protein cage.
  • The various genomes include 70-200 predicted open reading frames, thus as to gene diversity theyare among the most complex human viruses.

There are 80 known herpesviruses, and 8 of them are known to cause infection in humans:

  • Herpes simplex virus (HSV) 1 and 2.
  • Varicella-zoster virus.
  • Epstein-Barr virus
  • Cytomegalovirus
  • Human herpes virus 6 (HHV6).
  • HHV8. 

Trivial name

and acronym

Formal name








target cells

Main sites

of latency

Herpes simplex

virus-1 (HSV-1)


herpesvirus 1


Cold sores

(herpes ulcers

Genital ulcers, related

skin lesions, keratitis,

encephalitis, meningitis


Sensory and

cranial nerve


Herpes simplex

virus-2 (HSV-2)


herpesvirus 2


Cold sores

(herpes ulcers)

Genital ulcers, as

HSV-1 but more rare


Sensory and

cranial nerve


Varicella zoster

virus (VZV)


herpesvirus 3


Possible oral

manifestation of

chicken pox and

herpes zoster

Chicken pox, herpes



Sensory and

cranial nerve



virus (EBV


herpesvirus 4


Hairy leukoplakia,






Epithelial and


Memory B-cells




herpesvirus 5






and epithelia



Roseola virus




6A and 6B



Roseola in infants




Roseola virus



herpesvirus 7



Roseola in infants


T-cells, epithelia

Kaposi’s sarcomaassociated




herpesvirus 8



Kaposi’s sarcoma



and epithelia


  • Spread through direct contact with contaminated saliva or other infected bodily secretions, asymptomatic shedders with HSV present in salivary secretions.
  • Person who do not have immunity resulting fromprevious contact with the virus.
  • The majority of oral HSV infections is caused by HSV1,
  • Primary oral HSV2 infections are result of oral-genital contact.
  • Mothers giving birth to children with primaryHSV are asymptomatic carriers without lesions.
  • In new born after 6 months of age, the incidence of primary HSV1 infection increases because mothers with antibody titers are protected by placentally transferred antibodies during the first 6 months of life.
  • The incidence of primary HSV1 infection reaches a peak between 2 and 3 years of age.
  • Incidence of primary HSV2 infection does not increase until the age whensexual activity begins.

Incubation period is 5 to 7 days (range 2 to 12) days.

Prodromal symptoms:

  1. Fever.
  2. Loss of apetite.
  3. Malaise.
  4. Myalgia.
  5. Within few days of prodromal symptoms, erythema and clusters of vesicles and/or ulcers appear on the hard palate, attached gingival and dorsumof tongue and non-keratinised mucosa of buccal and labialmucosa, ventral tongue and soft palate.
  6. Vesicles break downto form ulcers that are usually 1–5 mm and coalesce to formlarger ulcers with scalloped borders and marked surroundingerythema.
  7. The gingiva is often fiery red, and the mouth isextremely painful, causing difficulty in eating.

Diagnosis of herpes virus infection made by:

  • Microscopy.
  • Antigen or DNA detection.
  • Virus isolation.
  • Serology.

Specimens include:

  • Vesicle fluid.
  • Skin swab.
  • Saliva.
  • Cor­neal scraping.
  • Brain biopsy and CSF according to site of involvement.
    1. Microscopy
      1. Tzanck’s smear:
        • Characteristic cytopathologic effects (CPEs) can be identified in a Tzanck smear (a scrap­ing of the base of a lesion), Papanicolaou smear (Pap), or biopsy specimen.
        • CPEs include syncytia, “balloon­ing” cytoplasm, and Cowdry type A intranuclear inclusions.
        • Smears are prepared from base of vesicles and stained with 1 percent aqueous solution of toluidine blue ‘0’ for 15 seconds.
        • Multi­nucleated giant cells with faceted nuclei and homogeneously stained ‘ground glass’ chromatin (Tzanck cells) constitute a positive smear.
      2. Electron microscopy: The virus particle may also be demonstrated under the electron microscope.
      3. Fluorescent antibody technique:
        • Herpesvirus antigen can be demonstrated in smears /sections from lesions by the fluorescent antibody technique.
        • Test on brain biopsy speci­mens useful in encephalitis.
    2. Virus Isolation
      • HSV isolates can be typed by biochemical, biologic, nucleic acid, or immunologic methods.
      • The restriction endonuclease cleavage patterns of the DNA of HSV-1 and HSV-2 and allow unequivocal typing of the isolates.
      • HSV type-specific DNA probes, specific DNA primers for PCR and antibodies are also useful.
    3. Serology

Antibodies develop within a few days of infection and rise in titer of antibodies demonstrated by ELI­SA, neutralization or complement fixation tests.

    1. Polymerase Chain Reaction

Useful for detecting viral DNA in cerebrospinal fluid when herpetic infection of the CNS is suspected.

Tzanck smear can be stained by: Hemacolorγ or Diff-Quikγ, hematoxylin and eosin, Wright, methylene blue, Papanicolaou and toluidine blue, Giemsa stain.

Recurrent herpes simplex infection, major apthous stomatitis, erythema multiformae.

  • HSV can cause neonatal infection intrapartum as the neonate comes into contact with the virus in the birth canal.
  • If transmission occurs in utero during the first trimester, the majority of fetuses will spontaneously abort.
  • Second or third trimester infection manifest as macroscopic physical signs such as cutaneous lesions, microcephaly, hydranencephaly, intracranial calcifications, chorioretinitis, microphthalmia and optic nerve atrophy, as well as microscopic changes including inflammatory changes to the infected tissues.
  • Any pregnant woman with suspected primary first episode HSV1 infection should undergo molecular testing by swabbing any lesions.

Type of infection



                                                                             Systemic HSV infection in adults

HSV encephalitis


10 mg/kg IVI q8h for 14-21 days

Disseminated HSV


5 mg/kg IVI q8h for 14 days

                                                                                      Genital HSV

Primary episode


400 mg potid x 7-10 days


1,000 mg po bid x 7-10 days


250 mg potid x 7-10 days

Recurrent episode

Episodic treatment


800 mg potid x 2 days or 400 mg potid x 5 days



1,000 mg bid x 1 day or 125 mg po

tid x 5 days



500 mg po bid x 3 days or 1 g daily

x 5 days

Daily chronic suppressive therapy


400 mg po bid



250 mg po bid



1 g podly

                                                                     Mucocutaneous HSV (oral labial, ‘fever blisters’)



2 g po bid x 1 day



500 mg po bid x 7 days



400 mg potid x 5 days

Neonatal HSV


Disseminated or CNS disease


20 mg/kg q8h for 21 days IVI

SEM(skin, eyes and mucosa) HSV disease


20 mg/kg q8h for 14 days IVI

  • If the serum sample is taken from an infected individual during the appearance of first clinical signs it is referred as acute sera.
  • A convalescent serum is serum which is collected from a person who is recovering from an infectious disease.
  • Stern used the term herpetic whitlow for the first time in 1959
  • The term “whitlow” is derived from the Scandinavian term “whichflaw”, meaning a crack in the sensitive area around the nail.
  • It is an acute viral infection of the hand caused by either herpes simplex virus (HSV) 1 or 2.
  • Infection usually occurs 3 to 7 days following exposure.
  • One or more vesicles appear around the nail, and they usually coalesce into large, honeycomb-like bullae in 5 to 6 days.
  • They may spread proximally and may also involve the nail bed.
  • The infection is usually self-limited and resolves in about 2 weeks.
  • Infection begins from an active lesion or infected secretions to the broken skin such as a torn cuticle of a finger or toe thus infecting the epithelial layer.
  • Following this, the virus replicates and forms vesicles on the finger.
  • Vesicles are usually clear or pale yellow, have a base which is erythematous, and can coalesce into a single vesicle.
  • Regional lymphadenopathy 
  • Made by the appearance of lesions and the patient’s history.
  • Viral culture can be sent by un-roofing vesicles and swabbing fluid at the base.
  • Vesicles contain the highest concentration of virus within the first 24 to 48 hour after they appear (89% positive).
  • PCR testing is much more sensitive.
  • Serology and direct fluorescent antibody testing.
  • Tzank test consists of scraping the floor of a herpetic vesicle, staining the specimen, and looking for multinucleated “balloon” giant cells.
  • Symptomatic relief and avoidance of secondary infection are the mainstays of therapy.
  • Antiretrovirals should be initiated within 48 hours and can be effective in recurrent infections if started during the prodrome.
  • Viral shedding is present until the epidermal lesion is healed, so patients should be counseled on the importance of wearing gloves or another protective barrier.

Flexor tenosynovitis, bacterial felon, and paronychia

  • Herpes labialis is a rash of the skin and mucous membranes (in particular, the lips) characterized by erythema and blisters that are preceded and accompanied by burning pain.
  • Contagious for individuals who have not been previously infected by the virus and for those with weakened immune systems like:
  1. HIV infection
  2. Undergoing chemotherapy.
  • Caused by herpes simplex virus type 1 (HSV-1).
  • Infection with type 2 virus can also lead to (primary) herpes labialis, but this type is rare.

Triggering factors are:

  • Trauma.
  • Sunburn.
  • Fever.
  • Emotional stress.
  • Systemic infection.
  • After primary infection, the virus recedes via the sensory nerve into the respective ganglion (usually the trigeminal ganglion), where it lies latent throughout the individual’s lifetime.
  • Stimuli can reactivate the virus, after which it returns to the epithelial cells via the sensory nerve.
  • Relapsing infections are limited to the mucosa of the hard palate or, in older children and adults, the lips.
  • The number of relapses decreases after the age of 35 years.
  • Lesions develop at the site of primary inoculation or in the adjacent area supplied by the involvedganglion.
  • Develop on the lips.
  • Lesionspreceded by a burning or tingling sensation anda feeling of tautness, swelling or slight soreness at the location.
  • Vesicles aregenerally small (1 mm or less in diameter), tend to occur inlocalized clusters, and may coalesce to form somewhat largerlesions.
  • These vesicles rupture quickly, leavinga small red ulceration, sometimes with a slight erythematoushalo.
  • On the lips, ruptured vesicles become covered bya brownish crust.
  • Young children often present with herpetic stomatitis, characterized by fever and the formation of small blisters and ulcers (2 to 10 mm) in the front of and around the mouth,tongueand lips.
  • Adults often present with sore throat and cervical lymph node swelling.

Indifferent cream

  • Zinc oxide and glycine cream (applied every 2 hours during the day).
  • Zinc sulfate (1%) gel (applied every 2 hours during the day).

Anesthetic cream

  • Lidocaine and prilocaine cream (25 mg of each per 1 g).

Antiviral cream

  • Acyclovir cream (5 times daily for 5 days).
  • Penciclovir cream to be applied every 2 hours during the day,

Oral antiviral medication

  • Acyclovir 400 mg 5 times daily for 5 days.
  • Valacyclovir, administered in either a 1-day (2000 mg twice daily) or a 2-day (2000 mg twice on the first day and 1000 mg twice on the second day).
  • Famciclovir (single 1500-mg dose or 750 mg twice daily for 1 day).
  • Also known as human herpes virus 3 is a ubiquitous alpha herpes virus with a double-stranded DNA genome.
  • VZV only naturally infects humans, with no animal reservoir; its main targets are T lymphocytes, epithelial cells and ganglia.
  • Primary infection causes varicella (chickenpox), during which VZV becomes latent inganglionic neurons.
  • As cellular immunity to VZV wanes with advancing age or in immunocompromised individuals, VZV reactivates to cause zoster (shingles).
  • Childhood disease.
  • Airborne disease. 
  • Disease is more severe in adults than in children.
  • Incubation period is about two weeks.
  • Symptoms begin 10 to 21 days after exposure.
  • Exposure causes the production of host immunoglobulin G, M, and A. IgG antibodies persist for life and confer immunity.
  • Chickenpox results in a skin rash that forms small, itchy blisters, which scabs over.
  • It typically starts on the chest, back, and face.
  • It is accompanied by fever, fatigue, pharyngitis, and headaches which usually last 5 to7days.
  • Pneumonia.
  • Brain inflammation.
  • Bacterial skin infections.

If infection occurs during the first 28 weeks of pregnancy, congenital varicella syndrome may develop. Effects on the fetus can include underdeveloped toes and fingers, structural eye damage, neurological disorder, and anal and bladder malformation.

Diagnosis isbased on:

  • Presenting symptoms
  • Polymerase chain reaction (PCR) testing of the blister fluid or scabs.
  • Blood tests to identify a response to acute infection (IgM), previous infection, and subsequent immunity (IgG).
  • Treatment is symptomatic.
  • Topical calamine lotion to relieve pruritus.
  • Daily cleansing with warm water will help avoid secondary bacterial infection. Acetaminophen to reduce fever.
  • Increasing water intake
  • Avoid aspirin as it may cause Reye syndrome.
  • In children, acyclovir decreases symptoms by one day if taken within 24 hours of the start of the rash.
  • In adults, infection tends to be more severe, and treatment with antiviral drugs (acyclovir or valacyclovir) is advised if they can be started within 24 to 48 hours of rash onset. 

After the primary disease is healed, VZV becomes latent in the dorsal root ganglia of spinal nerves or extra medullary ganglia of cranial nerves.

  • Herpes zoster (HZ) is a viral disease caused by endogenous reactivation of an infection by the varicella-zoster virus (VZV).
  • Characterized by an acute segmental (dermatomal) eruption of herpetiform vesicles on the skin and/or mucosa.
  • HZ is also known as shingles, which is derived from the Latin cingulum, meaning ‘girdle’.
  • This is because a common presentation of HZ involves a unilateral rash that can wrap around thewaist or torso like a girdle.
  • The name zoster is derived from classical Greek, referring to a belt-like binding (known as azoster) used by warriors to secure armour.
  • Zoster sine herpete (ZSH) refers to a condition in which dermatomal distribution pain occurs in the absence of an antecedent rash.

This is of two types:

  • Sclerotomal pain: A deep boring or twisting pain arising in muscles, joints, ligaments, etc., usually associated with tenderness of these structures to pressure.
  • Dermatomal pain: A superficial, burning or prickling pain, usually with associated hyperaesthesia, arising in or near the skin and termed “dermatomalpain.”

Patients at high risk:

  1. Immunocompromised due to HIV disease.
  2. Cancer chemotherapy.
  3. Immunosuppressive drug therapy.
  4. Hematologic malignancy.
  • Affect the individuals above 45 years of age (high 68 and 90 years).
  • Ophthalmic division is most commonly involved followed by the maxillary and mandibular divisions.
  • HZ follows a prodromal, active and chronic stage.
  • It presents with a prodrome of mild-to-moderate burning or tinglingor numbness in the skin of a given dermatome, often associated with fever, headache, generalmalaise and stomach upset.
  • About 48–72 h from the prodrome, there is development of a unilateral erythematous, maculopapular rash along the dermatome, which eventually develops into a vesicular lesion, this represents the active stage.
  • Pain varies in intensity from mild to severe in such a way that even the slightest stimuli can elicit excruciating spasms.
  • The lesions usually begin to dry and crustations appear after 3–5 days.
  • Total duration of the disease is generally between 7 and 10 days.
  • It may take several weeks for the hypopigmented skin to return to normal.
  • If the geniculate ganglion is involved, it may result in James Ramsay Hunt’s syndrome, which includes facial paralysis and painful vesiculareruptions of the external auditory meatus and pinna of the ear.
  • Chronic pain syndrome stage, termed post herpetic neuralgia (PHN).
  • Scarring of skin, keratitis, retinal necrosis causing blindness, keratouveitis, cranial and peripheral nerve palsies, cerebral ataxia and pneumonia may lead to death.
  • β-haemolytic streptococcal infections including cellulitis and necrotising fasciitis.
  • Periapical lesions, root resorption, tooth exfoliation and alveolar osteonecrosis.


Affected nerve



Zoster opthalmicus

First trigeminal nervebranch



Uveitis anterior, orbital phlegmon, retinal necrosis, superior orbital fissure syndrome,blindness

Zoster oticus

Vestibulocochlear and facial nerve

Pain localized to ear may also be affected

Bell’s palsy

Ramsay Hunt syndrome

Vestibulocochlear and facial nerve

Vesiculation in auditory canal, buccal mucosa, cheeks

Tinnitus, hearing loss, laryngitis, failure of lid closure

  • Self-limiting disease, early institution of antiviral and symptomatic therapy reduces the morbidity.
  • Antiviral treatment should be instituted within 72 h of cutaneous eruption, because most virus replication ceases 72 h after onset of rash.
  1. Acyclovir – 800 mg every 4 hours (five times daily) for 7 to 10 days.
  2. Famciclovir – 500 mg every 8 hours (three times daily) for 7 days.
  3. Valacyclovir- 1,000 mg every 8 hours (three times daily) for 7 days

Immunocompromised persons requiring hospitalization or severe neurologic Complications:

  1. Acyclovir (Intravenous) 10 mg/kg IV every 8 hrs × 7–10 days
  2. Foscarnet+ (for acyclovir-resistant VZV) 40 mg/kg every 8 hr until healed.

Medications commonly used for treatment of acute pain associated with herpes zoster:

  1. Analgesics-opioid and non-opioid
  2. Oxycodone – 5 mg every 4 hrs as needed.
  3. Tramadol – 50 mg once or twice daily.


Prednisone 60 mg daily for 7 days, then decrease to 30 mg daily for 7 days, then decrease to 15 mg daily for 7 days.


  1. Gabapentin 300 mg at bedtime or 100–300 mg 3 times daily.
  2. Pregabalin: 75 mg at bedtime or 75 mg twice daily.

Tricyclic anti depressants:

  • Nortriptyline 25 mg at bedtime.

Topical therapy:

Lidocaine 5% patch (Lidoderm®):  One patch topically for up to 12 hours to intact skin only

  • These are ribonucleic acid (RNA) entero viruses.
  • Named on town in upper New York State.
  • Entero viruses are small, non-enveloped, single positive-strand RNA viruses.
  • They are capable of surviving in a wide pH range.
  • They retain infectivity in temperatures up to 500
  • They are separated into two groups: A and B.
  • There are 24 known types of Coxsackie virus group A and 6 types of Coxsackie virus group B.
  • These viruses cause hepatitis, meningitis, myocarditis, pericarditis and acute respiratory disease. 

Group A Coxsackie viruses responsible for 3 clinical types of infection of the oral region:

  • Herpangina.
  • Handfoot- and-mouth disease.
  • Acute lymphonodular pharyngitis.
  • Coxsackie virus A1-6, 8, 10, and 22 are associated with Herpangina.
  • Transmission: Ingestion of infected saliva, respiratory droplets, or direct contact with fluid from vesicles.
  • Incubation period ranges from 3 to 5 days.
  • Viral shedding can occur even in asymptomatic patients. 
  • Infection begins with generalized symptoms of:
  1. Fever(1050 F)
  2. Chills.
  3. Anorexia.
  4. Sore throat.
  5. Dysphagia.
  6. Sore mouth.
  • Herpangina is associated with a stereotypical vesicular/ulcerative painful enanthem occurs on the soft palate, tonsils, and posterior pharynx.
  • Characterized by vesicles that eventually transition to tiny yellow or white ulcers with red rims.
  • Ulceration usually occurs within 24 hours after the appearance of vesicles.
  • These ulcers are generally 3 to 4 mm in diameter.
  • The rash preceded by an abrupt onset of fever.
  • Uncontrolled fevers sometimes provoke febrile seizures.
  • Lesions rarely develop on the buccal mucosa, tongue, and hard palate.
  • Disease is usually mild and heals without treatment in 1 week.
  • Herpangina occurs in epidemics; HSV infections do not.
  • Herpangina tends to be milder than HSV infection.
  • Lesions of herpangina occur on the pharynx and posterior portions of the oral mucosa but HSV primarilyaffects the anterior portion of the mouth.
  • Herpangina does not cause a generalized acute gingivitis like that associated with primary HSV infection.
  • Lesions of herpangina tend to be smaller than those of HSV.
  • Viral culture (take longer than 1 week to obtain culture results).
  • Polymerase chain reaction (fast and highly sensitive).
  • Samples may be obtained from the stool, mucocutaneous ulcers, vesicular fluid, or cerebrospinal fluid.
  • Enzyme-linked immunosorbent assays (ELISA) testing for enteroviruses is generally less sensitive than PCR.
  • Herpangina is a self-limiting disease.
  • Treatment is primarily supportive.
  • Ibuprofen:
  1. 6 to 11 months; 12 to 17 pounds: 50 mg (1.25 mL) every 6 to 8 hours
  2. 12 to 23 months; 18 to 23 pounds: 75 mg (1.875 mL) orally every 6 to 8 hours
  3. 2 to 11 years: 5 to 10 mg/kg orally every 6 to 8 hours.
  • Acetaminophen:
  1. Infants (29 days to 2 years old): 15 mg/kg every 6 hours
  2. 2 to 12 years: 12.5 mg/kg IV every 4 hours OR 15 mg/kg IV every 6 hours
  • Adequate oral hydration.
  • Intravenous immunoglobulin (IVIG).

Herpes simplex gingivostomatitis, aphthous ulcers, drug eruption, erythema multiforme major, eczema herpeticum, toxic shock syndrome, insect bites.

  • HFMD is caused by Coxsackievirus A16 and Enterovirus A71.
  • HFMD is identified by a similar rash on the oral mucous membranes, with additional characteristic exanthem on hands and feet.
  • Spread by oral ingestion of the shed virus from the gastrointestinal or upper respiratory tract of infected hosts, or via vesicle fluid or oral secretions.
  • After ingestion, the virus replicates in the lymphoid tissue of the lower intestine and the pharynx and spreads to the regional lymph nodes.
  • Can be spread to multiple organs including the central nervous system, heart, liver, and skin.
  • Age ranges from 8 months to 33 years,with 75% of cases occurring below 4 years of age.
  • Clinical manifestations lasted 3 to 7 days that start with:
  1. Low-grade fever.
  2. Reduced appetite.
  3. General malaise.
  4. Mouth or throat pain secondary to the enanthem.
  • Vesicles surrounded by a thin halo of erythema, eventually rupturing and forming superficial ulcers with a grey-yellow base and erythematous rim.
  • The exanthem can be macular, papular or vesicular.
  • The lesions are non-pruritic, and typically not painful.
  • The exanthem involves the dorsum of the hand, feet, buttocks, legs, and arms.
  • Usually made clinically.
  • The virus can be detected in the stool for about 6 weeks after infection.
  • Shedding from oropharynx is usually less than 4 weeks.
  • Light microscopy of biopsies or scrapings of vesicles.
  • Levels of IgG can be used to monitor recovery.
  • Polymerase chain reaction (PCR).
  • Hand, foot, and mouth disease is a mild clinical syndrome and will resolve within 7 to 10 days.
  • Treatment is primarily supportive.
  • Pain and fever can be managed with NSAIDs and acetaminophen.
  • Well hydration is important.
  • Mixture of liquid ibuprofen and liquid diphenhydramine can be used to gargle.

Herpes simplex gingivostomatitis, aphthous ulcers, drug eruption, erythema multiforme major, eczema herpeticum.

  • It is an acute febrile disease.
  • First reported by Steigman and coworkers in 1962.
  • Caused by a strain of Coxsackie virus A10.
  • Affects children and young adults.
  • Sore throat.
  • Fever (100°–105° F).
  • Mild headache.
  • Anorexia.
  • The symptomatic course varies from 4–14 days.
  • Local lesions resolve within 6–10 days.
  • A residual ring of fading erythema may sometimes be seen for several days.
  • Incubation period 2–10 days.
  • Raised, discrete, whitish or yellowish to dark pink solid papules or nodules, surrounded by a narrow zone of erythema.
  • The lesions are not vesicular and do not ulcerate.
  • The lesions appear on the uvula, soft palate, anterior pillars, and posterior oropharynx.
  • Isolation of Coxsackie A10 virus.
  • Serologic evidence of infection by this virus is also positive.

The disease is self-limiting and only supportivecare is indicated.

  • Also known as Rubeola, red spots, morbilli.
  • It is an RNA virus, belonging to the Morbilli virus genus, which is in the Paramyxoviridae
  • Humans are the only natural host of this highly contagious virus.
  • Transmitted through droplet nuclei.
  • Incidence is highest in late winter and spring (in temperate regions).
  • Afterinvasion of respiratory epithelium it reaches reticulo-endothelial system through blood stream andthereby infect skin, respiratory tract, and other organs.
  • Invasion of T lymphocytes and increased levels of suppressive cytokines leads to transient suppression of cellular immunity.
  • Monocyte is mainly infected.
  • Symptoms occur due to infection of the entire respiratory epithelia and secondary infection.

There are three stages:

  1. Pre-eruptive stage or prodromal stage.
  2. Eruptive stage
  3. Post eruptive stage.
  • Prodromal stage occurs 10 to 12 days after exposure and is characterized by two to three days of fever, anorexia, and malaise combined with the triad of cough, conjunctivitis, and coryza.
  • At the end of the prodromal stage, Koplik’s spots, an enanthem comprised of blue-white spots, appear on the buccal surfaces of the mouth and lasts 12 to 18 hours.
  • The prodromal phase is followed by the appearance of a maculopapular, erythematous rash, accompanied by high fever.
  • The rash occurs anywhere from 1 or 2 days before to 1 or 2 days after the Koplik’s spots appear, lasting five to six days.
  • The rash begins (and disappears) on the head and face, expanding outwards and downwards, eventually reaching the hands and feet.
  • A persisting cough characterizes the convalescent stage, which may persist up to one to two weeks after the rash resolves.
  • Has adverse maternal and fetal effectsduring pregnancy.
  • These are white papules resembling table salt like crystals with red base, appear on the buccal mucosa opposite to first and second molar teeth.
  • These characteristic spots are small, irregularly shaped flecks which appear as bluish, white speckssurrounded by a bright red margin.
  • These macular lesions increasein number rapidly and coalesce to form small patches.
  • This cell is found in lymph nodes or throughout the reticulo-endothelial system and diagnostic of measles.
  • The cell contains anywhere from a few to many small nuclei arranged in small morules or in a “grape-like” cluster, surrounded by a small amount of eosinophilic or basophilic cytoplasm.
  • Seropositive antibody response using a serological assay.
  • Detection of measles in clinical specimens (e.g., urine, nasopharyngeal secretions, throat swabs, or blood) by viral culture.
  • Specimens should be collected no later than seven to ten days after the rash onset.
  • Serological assays (e.g., enzyme-linked immunosorbent assays [ELISA], hemagglutination inhibition assays [HIA]) that measure IgM titers.
  • IgM capture assay can only be performed within 72 hours after rash onset.
  • Immune globulin is a recommended prophylaxis for non-immune, exposed obstetric patients.
  • Immune globulin is administered intramuscularly at 0.25 ml/kg (maximum dose = 15 ml; given at two injection sites).
  • It may suppress the measles-induced symptoms and if the maternal infection is close to parturition, it may reduce the risk of the neonate developing measles.
  • MMR Vaccine: The Edmonton–Zagreb (E-Z strain) 5 ml of vaccine is given subcutaneously at age of nine months.
  • A second dose should be given in the form of MMR at 15–18 months.
  • Also known as German measles.
  • Is an RNA virus in the genus Rubivirus within the Togaviridae
  • It is a human disease with no animal reservoirs.
  • Incidence is highest from late winter to early spring.
  • A prodromal stage of 1 to 5 days is represented by a low-grade fever, malaise, lymphadenopathy and an upper respiratory infection.
  • Forchheimer spots (petechiae on the soft palate) may precede or accompany the rash.
  • The rash is mild and maculopapular, beginning on the face and extending downwards; it occurs approximately 14 to 17 days after exposure and typically lasts three days.
  • Rubella frequently leads to arthralgia/arthritis in women.
  • Joint symptoms, along with conjunctivitis, are complications in the obstetric patient. Encephalitis may develop.
  • When rubella virus infects the fetus – particularly during the first trimester can lead to miscarriage or congenital rubella syndrome (CRS).
  • In CRS, rubella virus is able to infect the placenta, spread to the fetus, and alter the function of multiple fetal systems by interfering with organ formation and causing systemic inflammation.

The defects associated with congenital rubella syndrome (CRS) most commonly affect the eyes (e.g., cataracts, microphthalmia, glaucoma, pigmentary retinopathy, chorioretinitis), hearing (e.g., sensorineural deafness), the heart (e.g., peripheral pulmonary artery stenosis, patent ductusarteriosus or ventricular septal defects), and the brain (e.g., microcephaly).

In rubella, Koplik’s spots do not occur and the oral mucous membranes are not usually inflamed, although the tonsils may be somewhat swollen and congested and red macules may appear on the palate.

  • Virus detection usually consists of throat swabs (TS), oral fluids (OF) or nasopharyngeal secretions.
  • By antibody detection in sera or oral fluids.
  • Detection of rubella virus-specific IgM by either IgM capture ELISA or indirect IgM ELISA is diagnostic test for recent postnatal infection.
  • Infection is confirmed by a positive IgM, a fourfold rise in IgG, or a positive culture.
  • There is no effective antiviral treatment for rubella.
  • Treatment of symptoms includes plenty of fluids and pain relief if required.
  • Paracetamol may be used to reduce fever and pain.


  • Exclude people with rubella from childcare, preschool, school and work until fully recovered or for at least 4 days after the onset of the rash.
  • Rubella is best prevented by the measles, mumps and rubella (MMR) combination vaccine or the measles, mumps, rubella and varicella (MMRV) combination vaccine. Most people who have two doses of a rubella-containing vaccine will be protected against rubella infection.
  • Vaccination after exposure will not prevent infection.
  • All health care and childcare staff (men and women) should be assessed for immunity to rubella and if not immune, should be immunised.

Pregnant women:

In addition to the above prevention points, all pregnant women:

  • Should be tested for immunity to rubella prior to, or during early pregnancy.
  • If found not to be immune, MMR vaccination is given after delivery of the baby but before discharge from the maternity unit.
  • Rubella vaccine should not be given to a woman known to be pregnant and pregnancy should be avoided for one month after vaccination.
  • Also called water warts.
  • It is a benign condition of the skin.
  • The skin lesions of molluscumcontagiosum are called mollusca.

Caused by double-stranded DNA poxvirus called Molluscum Contagiosum virus (MCV).

Four subtypes:

  • MCV-1: Seen in children.
  • MCV-2: Responsible for skin lesions in HIV people
  • MCV-3 and MCV-4: Present in Asia and Australia.
  • Currently, it is not possible to have cultures of Molluscum Contagiosum virus.
  • Transmitted by direct skin-to-skin (including sexual) or indirect (towels, underclothes, toys, razor, tattoo supplies) contact.
  • By autoinoculation to normal skin after mollusca scraping by the patients.
  • From sharing swimming pools and other wet environments
  • MCV produces proteins inhibiting human antiviral immunity, thus preventing the development of innate immunity response, and contributing to the persistence of skin lesions.
  • Incubation period ranges from 2 weeks to 6 months.
  • MCV infects only keratinocytes and skin lesions are limited to the epidermis.
  • It does not have systemic dissemination.
  • Lesions are firm, white to flesh-colored, dome-shaped, pearly papules, having a central umbilication from which one can express a cheesy material.
  • Mollusca is usually one millimeter to one centimeter in diameter.
  • In children, mollusca are located on the face, trunk, limbs and axillary areas.
  • In sexually transmitted forms, lesions are mainly observed in the anogenital area, abdomen, and inner thighs.
  • There are rarely more than 20 to 30 elements over the skin and are usually grouped together.

Lesions may be atypical, have a greater size, and/or mimic malignancies, such as basal cell carcinoma or keratoacanthoma (for single lesions), or other infectious diseases, such as cryptococcosis and histoplasmosis (for extensive lesions).

  1. Dermoscopy.
  2. Reflectance confocal microscopy.
  3. Histopathology.
  • Dermoscopy of a molluscum shows a central white to a yellow amorphous area, with peripheral linear or branched vessels.
  • Reflectance confocal microscopy shows a well-defined central area, which contains septa separating hypo-refractive roundish lobules.
  • Histopathologically, enlarged keratinocytes having an abundant cytoplasm containing viral inclusions (also called Henderson Paterson bodies) and a peripheral nucleus. 
  • Physical removal is based mainly on cryotherapy with liquid nitrogen or curettage.
  • Laser treatment (carbon dioxide or pulsed dye laser).
  • Topical treatments:
  1. Podophyllotoxin (contraindicated in pregnant women).
  2. Potassium hydroxide.
  3. Salicylic acid (associated or not with povidone iodine).
  4. Benzoyl peroxide.
  5. Tretinoin.
  • Cidofovir, a DNA polymerase inhibitor, used in immunosuppressed persons.
  • Patients with HIV/AIDS best managed with highly active antiretroviral therapy (HAART).
  • Also known as Verruca acuminata, venereal wart.
  • Viral, sexually transmitted disease.
  • Caused by HPV which affects the genitalia, perianal region, rectal and urethral mucosae, and sometimes the oral cavity.
  • Condyloma acuminatum is caused by HPV type 6, a11, a30, b42, 43, 45, 46b 51, b54, 55, and 70.
  • Infection is usually transmitted by sexual intercourse 
  • Human papillomaviruses are members of the Papovaviridae family of epitheliotropic double-stranded DNA viruses.
  • These are considered tumor viruses because of their ability to immortalize normal cells.
  • Currently more than 130 types of HPV have been identified, with more than 40 types infectious for the lower genital tract, of which 15 are oncogenic.
  • These are characterized as:
  1. “Low-risk” types (6, 11, 42, 43, 44), which are primarily associated with genital warts and respiratory papillomatosis.
  2. “High-risk” types (16, 18, 31, 33, 35, 39, 45, 51, 52) are associated with low-grade and high-grade squamous intraepithelial lesionsand invasive cancer.
  • Both sexes are affected equally.
  • Peak incidence occurs in people in their 20s.
  • Incubation period after exposure ranges from one to twenty months (average 2 to 3 months).
  • Perianal growth.
  • Pruritus ani.
  • Discharge.
  • Bleeding.
  • Odor.
  • Tenesmus.
  • Difficult perianal hygiene
  • Affect the mucosa of the gingiva, cheeks, lips, and hard palate. 
  • Lesions appeared as small, multiple, white or pink nodules.
  • Nodules become enlarge, proliferate and coalesce, or as papillomatous, bulbous masses.
  • Physical examination may reveal the classic cauliflower-like lesion.
  • Histopathological examination.
  • Serologies and cultures for HPV.
  • PCR technique can be used to detect HPV DNA with high sensitivity.
  1. 1.   Topical Chemical Agents

    A.   Podophyllin

    ·         Topical chemical agent.

    ·         Cytotoxic agent derived from the resin of Podophyllum emodi and Podophyllum peltatum that contains biologically active lignin compounds, including podofilox, which is the best-characterized and most active component against genital warts.

    ·         Applied in a vehicle such as liquid paraffin or tincture of benzoin.

    ·         Podophyllin is applied directly to the warts with care to avoid the adjacent normal skin because it is extremely irritating.

    ·         Use during pregnancy associated with teratogenicity and intrauterine fetal death.

    B.   Bichloracetic Acid Or Trichloracetic Acid

    ·         Powerful keratolytic and cauterant.

    ·         It is inexpensive and easily applied.

    ·         Can cause local skin irritation and often requires multiple office visits, generally at weekly intervals.

    C.   Chemotherapeutic Agents

    5-fluorouracil (5-FU) as a cream or salicylic acid preparation,thiotepa, bleomycin, dinitrochlorobenzene in acetone, and idoxuridine cream.

    2.   Immunotherapy

    A.   Interferon

    ·         Interferons are produced and secreted in response to viral infections. Thus interferon injection may be a practical way to treat refractory anogenital warts.

    ·         Intramuscular, intralesional, and topical therapies are available.

    ·         The usual dose of intralesional interferon is 1 to 2 million units.

    ·         10 to 28 days of daily treatment is required.

    ·         Maximum dose per patient is 5 million units.

    ·         Adverse effects: Fever, chills, myalgia, headache, fatigue, and leukopenia.

    B.   Imiquimod

    ·         Topical imiquimod is an immune modulator that induces interferon and cytokine release by the host tissues.

    ·         Applied as a 5% cream.

    C.   Vaccine

    ·         In 1944, Biberstein first described the use of immunotherapy with an autologous vaccine in the treatment of condylomata acuminatum.

    ·         HPV vaccines targeting the late structural proteins of the viral capsid (E6, E7) have shown more promise.

    ·         The ideal vaccine engenders a cell-mediated immune response generating HPV-specific cytotoxic T-lymphocytes.

    3.   Surgical Therapy

    A.   Electrocoaguation

    ·         Electrocautery is an effective way to destroy both internal and external anal warts but this technique requires local anesthesia.

    ·         The effect is a first- or second-degree burn.

    ·         Controlling the depth of the wound is important to prevent scarring and injury to the underlying anal sphincters.

    B.   Laser Therapy

    Carbon dioxide laser therapy is useful.

    C.   Cryotherapy

    Cryotherapy involves the topical application of liquid nitrogen, carbon dioxide snow, or liquefied air to the warts.

    D.  Surgical Excision

    ·         Classically a solution of 1:200,000 epinephrine in saline or lidocaine is injected subcutaneously and submucosally to separate the warts and facilitate the preservation of healthy skin and mucosa.

    The combination of excision and electrocautery is considered to be the gold standard for the treatment of condylomata.

  • Also known as Variola.
  • Smallpox is a member of the viral family poxvirus, genus orthopoxvirus, and species variola virus.
  • Poxviruses possess a linear, double-stranded DNA genome.
  • Transmission occurs through airborne respiratory droplet secretions.
  • By direct contact with lesions or contaminated fomites.

After entry through the oropharynx or nasopharynx, the virus migrates to regional lymph nodes where it begins replication. 

  • Initial viremia: Occurs on day 3 to 4 after infection, and the virus further disseminates to the bone marrow, spleen, and additional lymph node chains.
  • Secondary viremia: Occurs between days 8 to 12 after infection and coincides with the onset of fever and clinical evidence of illness. At this stage, the virus becomes localized in the oropharyngeal mucosa and small blood vessels of the dermis, resulting in the onset of rash and clinical infectiousness.
  • High fever.
  • Malaise.
  • Prostration with headache.
  • Delirium.
  • Severe abdominal pain.
  • Around day 14, a maculopapular rash appears on mouth and pharynx, face, forearms and spreads to the trunk and legs.
  • Characteristicrash had a centrifugal appearance and most prominent on the face and the extremities, including the palms and soles.
  • Lesions typically appear during a 1- to 2-day period.
  • Smallpox is most infectious during the first week of the rash.
  • Complications of smallpox infections were secondary bacterial infections, meningitis, and encephalitis.
  • Ulceration of the oral mucosa, pharynx,trachea, esophagus, and vagina
  • Multiple vesicles that rupture and form ulcers of a nonspecific nature.
  • Hemorrhagic-Type– Associated with petechiae in the skin and bleeding from the conjunctiva and mucous membranes.
  • Associated with very severe toxemia and high mortality rates, often in early stages of disease development.
  • Flat-Type – Characterized by severe toxemia and delayed onset and slow development of skin lesions. Most of these cases were fatal.
  • Modified-typeSeen in patients who had been previously vaccinated. Skin lesionsusually evolved quickly and were more variable in their appearance.
  • Virus culture
  • Immunohistochemistry
  • Electron microscopy
  • Various polymerase chain reaction techniques
  1. Essential conserved genes (E9L, A25R)—difficult to discriminate among species of orthopox viruses.
  2. Nonessential, variable genes (HA, HTI, crmB)—species specific
  • Serology
  1. Antigen detection (immunofluorescent assay, enzyme immunoassay, antigen capture).
  2. Neutralization antibodies.
  3. Immunoglobulin M capture.
  4. Immunoglobulin G enzyme-linked immunosorbent assay.
  • There is no proven treatment.
  • Some antiviral drugs may help treat it or prevent it from getting worse.
  • There also is a vaccine to protect people from smallpox.

Smallpox Vaccine

  1. Smallpox can be prevented by the smallpox vaccine.
  2. If person get the vaccine:
  • Before contact with the virus, the vaccine can protect from getting sick.
  • Within 3 days of being exposed to the virus, the vaccine might protect from getting the disease. If person still get the disease, he might get much less sick than an unvaccinated person would.
  • Within 4 to 7 days of being exposed to the virus, the vaccine likely gives some protection from the disease. If person still get the disease, he might not get as sick as an unvaccinated person would.

Once person have developed the smallpox rash, the vaccine will not protect him.

  1. Antiviral Drugs

Tecovirimat: recommended dose of tecovirimat in adult and pediatric patients who weigh-

  • Above 13 kg to below 25 kg: One capsule (200 mg) two times daily.
  • Above 25 kg to below 40 kg: Two capsules (400 mg) twice daily.

• 40 kg and above: Three capsules (600 mg) two times daily.

  • Chikungunya virus (CHIKV) is an arbovirus transmitted to humans by Aedes mosquitoes.
  • The virus was first described in 1952 during a febrile illness outbreak in Makonde, a province in southern Tanzania.
  • The word chikungunya comes from the Bantu language of the Makonde ethnic group from Tanzania and Mozambique.
  • It is a mosquito-borne alpha-virus that is characterized by the triad: fever, arthralgia and rash.
  • Chikungunya is a positive-sense single-stranded RNA virus that is approximately 12 kb in length.

The genome has two open reading frames (ORFs): the 5´ORF, translated from genomic RNA, encodes the nsP1, nsP2, nsP3, and nsP4 non-structural proteins, and the 3´ORF, translated from subgenomic RNA, encodes a polyprotein that is processed into the structural proteins [capsid (C), envelope (E1 and E2), and two peptides (E3 and 6K)]

  • CHIKV is transmitted to humans by mosquitoes of the genus Aedesspp, particularly Aedesaegypti.
  • Aedes albopictusis the second-largest transmitter of CHIKV.
  • Other species transmit CHIKV: Eretmapodites chrysogasterCulex annulirostrisMansonia uniformis, Anopheles stephensi, and Opifexfuscus

Chikungunya classified into three phases:

  • Acute.
  • Post-acute.
  • Chronic.

Acute phase:

  • This phase is considered the first three weeks of the disease, i.e., the first 21 days of clinical manifestations.
  • After an incubation period (2-4 days) patient exhibit:
    1. High fever.
    2. Polyarthralgia/polyarthritis.
    3. Intense myalgia, accompanied by:
      1. Headache.
      2. Photophobia.
      3. Rash.
      • Polyarthralgia affects limb joints symmetrically and bilaterally and they are typically swollen.

Skin manifestations:

      • These manifestations appear after the arthralgia and myalgia.
      • Macular and maculopapular exanthemas.
      • Diffuse erythema with or without pruritus.
      • Facial oedema.

Other cutaneous-mucosal lesions:

      • Vesicles
      • Blisters.
      • Exfoliative dermatitis.
      • Erythema nodosum.
      • Hyperpigmentation.
      • Photosensitivity.
      • Exacerbation of existing dermatoses.

This phase begins after the 21st day of clinical manifestations and continues for 3
Clinical manifestations:

  • Arthralgia.
  • Arthritis (synovitis with or without effusion).
  • Tenosynovitis.
  • Bursitis.
  • Enthesitis.
  • Periostitis.
  • Tendinitis, with the risk of tendon rupture.
  • Morning joint stiffness.
  • Neuropathic pain.
  • Peripheral vascular phenomena.

• The disease is considered chronic when the arthralgia persists for more than three months.
• Arthralgia and arthritis tend to be bilateral and symmetrical and may be migratory, with pain assuming an intermittent or constant characteristic, possibly accompanied by articular oedema or morning joint stiff.
• When oedema occurs, redness and heat are usually not present.
Musculoskeletal manifestations:
• Tenosynovitis.
• Typically, two or more tendons are affected.
• Wrist, finger, and ankle extensors and flexors.
• Patients with hypertrophic wrist tenosynovitis complain of nocturnal paraesthesia in the fingers.

• Maculopapular rashes.
• Gingival hemorrhages.
• Gingival bleeding.
• These signs are more frequentin children.

Diagnosis based on:
• Viral isolation.
• Viral RNA identification by reverse transcription (RT) and real-time PCR
• Detection of IgM and IgG antibodies through serological tests using enzyme linked immunosorbent assays (ELISA) and/or rapid immunochromatographic tests.

Mild-intensity pain (VAS from 1 to 3):

Dipyrone and paracetamol.

Adult: Weighing more than 60 kg, dipyrone at a dosage of 1.0 g every 6 h.

Paracetamol at dosages of 500–750 mg every 4–6 h, not exceeding the maximum daily dosage of 4.0 g due to the risk of hepatotoxicity.

Moderate-intensity pain (VAS from 4 to 6)

Dipyrone and paracetamol should be prescribed together in the same fixed dosages (6/6 h), alternating their administration every 3 h.

Severe neuropathic pain:

  • 25 or 50 mg of amitriptyline hydrochloride combined with the analgesic (dipyrone or paracetamol).
  • 300 mg of gabapentin twice a day (total of 600 mg/day), with a maximum dosage of 1,200 mg/day or75 mg of pregabalin twice a day as the starting dose, which may be increased to a maximum dosage of 600 mg/day (300 mg twice a day).

Severe-intensity pain (VAS from 7 to 10) – 

Tramadol hydrochloride at a dosage of 50–100 mg orally every 6 h and 30 mg of codeine combined with paracetamol (500 mg) every 6 h.

Pregnant women:

  • Paracetamol, the dose should not exceed 4 g/day.
  • From the 24th week of gestation onwards, all NSAIDs (including aspirin and topical NSAIDs) are contraindicated due to the risks of foetal renal failure and closure of the ductus arteriosus.

• The human immunodeficiency virus (HIV) is grouped to the genus Lentivirus within the family of Retroviridae, subfamily Orthoretrovirinae.
• On the basis of genetic characteristics and differences in the viral antigens, HIV is classified into the types 1 and 2 (HIV-1, HIV-2).

In 1986, Dr. Suniti Solomon diagnosed the first HIV case in the city of Chennai, in a female sex worker.

  • HIV is a type of lentivirus, which means it attacks the immune system. In a similar way, the Simian Immunodeficiency Virus (SIV) attacks the immune systems of monkeys and apes.
  • Research found that HIV is related to SIV and there are many similarities between the two viruses. HIV-1 is closely related to a strain of SIV found in chimpanzees, and HIV-2 is closely related to a strain of SIV found in sooty mangabeys.

AIDS is caused by an RNA (retrovirus) virus called human immunodeficiency virus (HIV). There are 4 members of human retroviruses in 2 groups:

  1. Transforming viruses: These are human T cell leukaemia lymphoma virus (HTLV) I and II and are implicated in leukaemia and lymphoma.
  2. Cytopathic viruses: This group includes HIV–1 and HIV-2, causing two forms of AIDS. Most common case of AIDS in the world including US is HIV-1, while HIV-2 is etiologic agent for AIDS in cases from West Africa and parts of India.

HIV is a spherical enveloped virus about 90-120 nm in size. The nucleocapsid has an outer icosahedral shell and inner cone-shaped core enclosing the ribonucleoproteins.

Genome: Genome is composed of two identical single-stranded, positive sense RNA copies with the reverse transcriptase enzyme (a characteristic feature of retroviruses). When the virus infects the cell, the viral RNA is transcribed by the enzyme, first into single-stranded DNA and then to double stranded DNA    (provirus) which is integrated into the host cell chromosome. The provirus can remain latent for long period, influencing host cell function.

Lipoprotein Envelope: When the naked virus buds out through the host cell surface during virus replication, it acquires a lipoprotein envelope which consists of lipid derived from the host cell membrane and glycoproteins coded by the virus. The major virus-coded envelope proteins are the projecting knob like spikes on the surface and the anchoring transmembrane pedicles. The spikes constitute the main surface component of the virus, which binds to CD4 receptors (along with co-receptors CXCR4 and CCR5) on susceptible host cells.

HIV genome contains the 3 structural genes as well as other non structural and regulatory genes specific to virus:
1. Major antigens of HIV
A. Envelope antigens
• Spike antigen- gp120.
• Transmembrane pedicle protein- gp41.
B. Shell antigen
• Nucleocapsid protein- p18.
C. Core antigens
• Principle core antigen p24.
• Other core antigen p15, p55.
D. Polymerase antigen p31 p51 p66
2. Non-structural and regulatory genes
• tat ( trans activating gene ).
• nef ( negative factor gene).
• rev ( regulator of virus gene).
• vif ( viral infectivity factor gene).
• vpu (only in HIV-1) and vpx (only in HIV-2).
• vpr.
• LTR (long terminal repeat) sequences.

There are two distinct types of human AIDS viruses: HIV-1 and HIV-2.

  • Based on envgene sequences.
  • HIV-1 comprises three distinct virus groups: M (for ‘major’), O (for ‘outlier’) and N (for new).
  • M Group

The predominant M group, which causes the large majority of HIV-1 infections worldwide, contains nine subtypes or “clades” (A-K, omitting E and I).

  • O Group

A few HIV-1 strains isolated from West Africa (Cameroon, Gabon) do not fall within the Group M and have been designated Group O.

  • N Group

Some recent isolates of HIV-1 from Cameroon, distinct from M and O groups have been called Group N.

• HIV strains, first isolated from West Africa in 1986, which reacts with HIV type 1 antiserum very weakly or not at all have been termed HIV type 2.
• HIV-1 and the chimpanzee virus carry a vpu gene, whereas HIV-2 and most Simian Immunodeficiency Virus (SIVs) have a vpx gene.
• Six subtypes of HIV-2 (A-F) have been identified.
• Subtype A is the most prevalent, being found worldwide.
• B is the most common in the Americas and Europe.
• The common subtypes in Af¬rica are A, C and D.
• In Asia the common subtypes are E, C and B.
• Subtype E is the commonest in Thailand.
• In India and China, subtype C is the most prevalent.

Through contact with infected body fluid like:

  • Blood.
  • Semen
  • Vaginal secretions.
  • Breast milk.
  • Transmission may occur across mucous membranes or broken skin during sexual intercourse (both heterosexual and homosexual).
  • Intravenous exposure like :

A. Sharing infected needles with intravenous drug use.

B.Occupational exposure in the health care environment.

C. Treatment with infected blood products.

• Yes, transmission of infection from mother to baby can take place by:
• Intrauterine transmission.
• Peripartum transmission.
• Breast feeding.

Infection is acquired when the virus enters the blood or tissues of a person and comes into contact with a suitable host cells, principally the CD4 lymphocytes.

Cell receptor for virus attachment: The receptor for the virus is any cell bearing CD4 antigen, primarily the CD4 + (helper/ inducer) T lymphocyte.

Specific binding of the virus to the CD4 receptor is by the envelope glycoprotein gp120. Cell fusion is essential for infection to take place. This is brought about by transmembrane gp41. Binding to the CD4 receptor requires the participation of a co-receptor molecule, which has been identified as CXCR 4 for T cell-tropic HIV strains and CCR 5 for macrophage tropic strains.

Replication: After fusion of the virus with the host cells membrane, the HIV genome is uncoated and internalised into the cell. Viral reverse transcriptase mediates the transcription of its RNA into double-stranded DNA, which is integrated into the genome of the infected cells through the action of the viral enzyme integrase, causing a latent infection. The long and variable incubation period of HIV infection is because of the latency.

Primary pathogenic mechanism: Is the damage to the CD4+T lymphocyte. The T4 cells decrease in numbers with the reversal of T4:T8 (helper: suppressor) cell ratio. Infected T4 cells do not release normal amount of interleukin-2, gamma interferon and other lymphokines, suppressing cell-mediated immune response.

Though the main damage is to cellular immunity, humoral mechanisms are also affected. Helper T cell activity is essential for optimal B cell function. AIDS patients are unable to respond to new antigens. An important feature in HIV infection is the polyclonal activation of B lymphocytes leading to hypergammaglobulinemia of all classes of immunoglobulins, particularly IgG and IgA. In infants and children, IgM levels are also elevated. The hypergammaglobulinemia may also be responsible for allergic reaction due to immune complexes (type 3 hypersensitivity).

Monocyte–macrophage function:  Is also affected, apparently due to lack of secretion of activating factors by the T4 lymphocytes. As a result, chemotaxis, antigen presentation and intracellular killing by monocytes/macrophages are diminished. The activity of NK cells and cytotoxic T lymphocytes is also affected.

The principal immunological abnormalities seen in HIV infection are as follows:

  • Features that characterize AIDS
    1. Lymphopaenia
    2. Selective T cells deficiency- Reduction in number of T4(CD4) cells, inversion of T4:T8 ratio.
    3. Decreased delayed hypersensitivity on skin testing.
    4. Hypergammaglobulinemia- Predominantly IgG and IgA; IgM also in children.
    5. Polyclonal activation of B cells and increased spontaneous secretion of Ig.
  • Other consistently observed features
    • Decreased in vitro lymphocyte proliferative response to mitogens and antigens.
    • Decreased cytotoxic response by T cells and NK cells.
    • Decreased antibody response to new antigen.
    • Altered monocyte/ macrophage function.
    • Elevated levels of immune complexes in serum.


The natural evolution of HIV infec­tion can be considered in the following stages:

Stage I—Acute HIV Infection

  • Within 3-6 weeks of infection, patient experiences:
  • Acute seroconversion illness that resembles glandular fever, adenopathy, flu-like symptoms.
  • Low grade fever.
  • Malaise.
  • Headache.
  •  Lymphadenopathy.
  • Spontaneous resolution occurs within weeks.
  • During this period high level of virus replication occurring in CD4+ cells.
  • Tests for HIV antibodies are negative at the onset of the illness but become positive during its course. Hence this syndrome called ‘seroconversion illness’.
  • HIV antigenemia (p24 antigen) can be demonstrated at the beginning of this phase.

Stage II—Asymptomatic or Latent Infection

  • Asymptomatic or “latent” period follows the acute infection.
  • High level of ongoing viral replication.
  • Positive HIV antibody tests.
  • The infection progresses in course of time through various stages, CD4 lymphocytopenia, minor opportunistic infections, persistent generalized lymphadenopathy, AIDS-related complex (ARC), ultimately terminating in full blown AIDS, with its characteristic infections and malignancies.
  • The time from infection to death may be as long as 10 years.


Stage III—Persistent Generalized Lymphadenopathy (PGL)

  • This has been defined as the pres­ence of enlarged lymph nodes, at least 1 cm in diameter, in two or more noncontiguous extrainguinal sites, that persist for at least three months, in the absence of anycurrent illness or medication that may cause lymphad­enopathy.
  • This by itself is benign but the cases may progress to ARC or AIDS.

Group IV—AIDS Related Complex (ARC)

  • This includes patients with considerable immunodeficiency, suffering from various constitutional symptoms or minor opportunistic infections.

Typical symptoms:

  1. Fatigue.
  2. Unexplained fever.
  3. Persistent diarrhea.
  4. Marked weight loss of more than 10 percent of body weight.

Common opportunistic infections:

  1. Oral candidiasis.
  2. Herpes zoster.
  3. Hairy cell leukoplakia.
  4. Salmonellosis.
  5. Tuberculosis.
  6. Generalized lymphadenopathy, splenomegaly is present.
  • ARC patients are usually severely ill and many of them progress to AIDS in a few months.
  • With no treatment, the interval between primary infectionand the first appearance of clinical diseaseis usuallylong in adults, averaging about 8-10 years. Deathoccurs about 2 years later.
  • The features classified as group IVinclude what was known as the AIDS-related complex or ARC.

The median time between primary HIV infection and development of AIDS is approx. 10 years.

• M. avium complex.
• Mycobacterium tuberculosis—disseminated or extra pulmonary.
• Salmonella—recurrent septicemia.
• Cytomegalovirus.
• Herpes simplex virus.
• Varicella-zoster virus.
• Epstein-Barr virus.
• Human herpes virus 6.
• Human herpes virus 8.
• Candidiasis.
• Cryptococcosis.
• Aspergillosis.
• Pneumocystis carinii pneumonia.
• Histoplasmosis.
• Coccidioidomycosis.
• Toxoplasomosis.
• Cryptosporidiosis.
• Lsosporiasis.
• Microsporidiosis.
• Generalized strongyloidiasis.
• Kaposi’s sarcoma
• B cell lymphoma or non-Hodgkin’s lymphoma
F. Slim Disease

  • Demonstration of antibodies may take place from 2-8 weeks to months after infection.
  • During this period, the individual may be highly infectious. This seronegative infective stage is known as “window period”. Hence, antibody testing is not totally dependable for detecting infectious person.
  • Testing for antibodies needs to be done only after 2-6 months to ascertain whether infection has occurred or not, after single sexual exposure.

HIV- HIV stands for human immunodeficiency virus. It is the virus that can lead to acquired immunodeficiency syndrome, or AIDS.HIV attacks the body’s immune system, specifically the CD4 cells (T cells), which help the immune system fight off infections. Untreated, HIV reduces the number of CD4 cells (T cells) in the body, making the individual more likely to get other infections or infection-related cancers.

AIDS- This is the end-stage disease representing the irreversible breakdown of immune defence mechanisms, leaving the patient prey to progressive opportunistic infections and malignancies.

  • Babies born to infected mothers are infected with HIV.
  • Infection is transmitted to the baby in the perinatal peri­od when the child’s immune system is immature.
  • Transmission can also take place during delivery or from breast milk.
  • Pediatric AIDS—acquired from infected mothers—usually presents with clinical symptoms by 2 years of age. Death follows in another 2 years.
  • Children may also acquire the infection from blood transfusion or blood products.
  • Early infant diagnosis done by testing for pro-viral DNA by PCR on blood collected from the newborn by heel prick and absorbed on dry filter paper. This dried blood is sent to a referral laboratory for testing.

Yes, the risk of mother-to-child transmission of HIV is low when:

  • HIV is detected as early as possible during pregnancy (or before a woman gets pregnant).
  • Women with HIV receive HIV medicines during pregnancy and childbirth and, in certain situations, have a scheduled cesarean delivery (sometimes called a C-section).
  • Babies born to women with HIV receive HIV medicines for 4 to 6 weeks after birth and are not breastfed.

The Centers for Disease Control and Prevention (CDC) recommends that all women who are pregnant or planning to become pregnant get tested for HIV early—before pregnancy, if possible, and during every pregnancy.

1. Strongly associated Lesions
A. Candidiasis
• Erythematous
• Pseudomembranous
B. Hairy leukoplakia
C. Kaposi’s sarcoma
D. Non Hodgkin’s lymphoma
E. Periodontal disease:
• Linear gingival erythema.
• Necrotizing (ulcerative) gingivitis.
• Necrotizing (ulcerative) periodontitis.
2. Less commonly associated lesions:
A. Bacterial infections
• Mycobacterium aviumintracellulare
• Mycobacterium tuberculosis
B. Melanotic hyperpigmentation
C. Necrotizing (ulcerative) stomatitis
D. Salivary gland disease
• Dry mouth due to decreased salivary flow rate
E. Unilateral or bilateral swelling of themajorsalivary glands
F. Thrombocytopenic purpura
G. Ulceration NOS (not otherwise specified)
H. Viral infections
• Herpes simplex virus
• Human papillomavirus (wart likelesions)
• Condyloma acuminatum.
• Focal epithelial hyperplasia.
• Verruca vulgaris.
• Varicella zoster virus.
• Herpes zoster.
• Varicella.
3. Lesions seen in HIV infection
A. Bacterial infections.
• Actinomyces Israel.
• Escherichia coli.
• Klebsiella pneumonia.
B. Cat scratch disease
C. Drug reactions (ulcerative, erythema multiforme, lichenoid, toxic epidermolysis).
D. Epithelioid (bacillary) angiomatosis.
E. Neurologic disturbances.
• Facial palsy.
• Trigeminal neuralgia.
F. Fungal infection other than candidiasis
• Cryptococcus neoformans.
• Geotrichumcandidum.
• Histoplasma capsulatum.
• Mucoraceae (mucormycosis/zygomycosis).
• Aspergillus flavus
G. Recurrent aphthous stomatitis
H. Viral infections.
• Cytomegalovirus.
• Molluscum Contagiosum.

  • Highly reactive.
  • Viral genome shed very fast.

1. Antigen Detection
• The major core antigen p24 is the earliest virus marker to appear in blood.
• The appearance of p24 antigenemia and viremia followed by IgM antibody response coincides with the acute or seroconversion illness.
• Afterwards, free p24 antigen disappears from circulation and remains absent during the long asymptomatic phase, to reappear only in severe clinical disease.
• The p24 antigen capture assay (ELISA) which uses anti-p24 antibody as the solid phase can be used for this.
• The test is most useful in persons recently exposed to risk of infection, in whom antibody test is negative.
2. Virus Isolation
• Virus is present in circulation and body fluids, within lymphocytes or cell-free.
• It can be isolated from CD4 lymphocytes of peripheral blood, bone marrow and serum.
• The technique of isolation is by co-cultiva¬tion of the patient’s lymphocytes with uninfected lym¬phocytes in the presence of interleukin-2.
• Virus pres¬ence is detected by assays for reverse transcriptase and p24 antigen in the culture fluids.
3. Detection Of Viral Nucleic Acid
• As the most sensitive and specific test.
• PCR has become the gold standard for diagnosis in all stages of HIV infection.
• Two forms of PCR have been used, DNA PCR and RNA PCR.
In the DNA PCR, peripheral lymphocytes from the sub¬ject are lysed and the proviral DNA is amplified using primer pairs from relatively constant regions of HIV genome.
• The HIV RNA by PCR test is used to provide a measurement of HIV genetic material in the blood.
• This is also known as a “viral load test.”
• HIV RNA testing is often used to determine how actively the HIV virus is reproducing in a person who has been diagnosed with HIV infection.
• This test can also be used to monitor the status of infection for a person who is undergoing retroviral therapy or whose HIV infection in a latent period.
4. Antibody Detection
• Antibodies may take 2 months to appear, if infection has taken place.
• Antibody testing will have to be done after 2-6 months to ascertain whether infection has occurred or not, after a single sexual exposure.
• Serological tests for anti-HIV antibodies are of two type:
A. Screening test
B. Confirmatory tests
Screening (E/R/S) tests
a. Enzyme-linked Immunosorbent Assays (ELISA) Tests
• Direct solid phase antiglobulin ELISA is the method most commonly used.
• T- Antigen is obtained from HIV grown in continuous T lymphocyte cell line or by recombinant techniques and should represent all groups and subtypes of HIV-1 and HIV-2.
• The antigen is coated on microtiter wells or other suitable solid surface.
• The test serum is added, and if the antibody is present, it binds to the antigen.
• After washing away the unbound serum, antihuman immunoglobulin linked to a suitable enzyme is added, followed by a color-forming substrate.
• If the test serum contains anti-HIV antibody, a photometrically detectable colour is formed which can be read by special ELISA readers.
b. Rapid Tests
• Dot blot assays.
• Particle agglutination (gelatin, RBC, latex, microbeads).
• HIV spot and comb tests.
• Fluorometric microparticle technologies.
• Tests using finger-prick blood, saliva and urine also available.
c. Simple Tests
• Not as fast as rapid tests.
• Take 1-2 hours and also do not require expensive equipment.
• Based on ELISA principle
5. Supplemental Tests
A. Western Blot Test
• In this test, HIV proteins, separated according to their electrophoretic mobility (and molecular weight) by polyacrylamide gel electrophoresis, are blotted onto strips of nitrocellulose paper.
• The antigen impreg¬nated nitrocellulose is then cut into strips, each strip having the full complement of vital proteins which were separated in the gel.
• Each strip is then incubated with a dilution of patient serum.
• Antibodies which attach to the separated viral antigens on the strip are detected by anti-human immunoglobulin antibody to which enzyme has been attached.
• The binding of this tracer antibody to the human immunoglobulin is detected by the addition of the enzyme conjugate followed by application of a substrate.
• The substrate changes color in the presence of enzyme and permanently stains the strip.
• The location or position on the strip at which a patient’s antibodies attach to viral antigens indicates whether antibody is specific for viral antigens or directed against non-viral material from the cells in which the virus was grown.
• WB results are scored as negative, positive, or indeter¬minate
B. Immunofluorescence Test
In this test, HIV infected cells are acetone fixed on to glass slides and then reacted with test serum followed by fluorescein conjugated anti-human gammaglobulin.
A positive reaction appears as apple-green fluorescence of cell membrane under fluorescence microscope.
6. Non-specific Tests
A. Immunological Tests
The following parameters help to establish the immunodeficiency in HIV infection:
• Leukopenia and a lymphocyte count usually below 2000/mm3.
• Absolute CD4+ T cell count less than 200/mm3.
• T4:T8 cell ratio is reversed (normal ratio is 0.9 to 1.9 in HIV negative).
• Thrombocytopenia.
• Raised IgG and IgA levels.
• Diminished CMI as indicated by skin tests.
• Lymph node biopsy showing profound abnormalities.

Some laboratory tests are important in monitoring the course of HIV infection.

  1. CD4+ T Cell Count
  • Reflects the current immunological competence of the patient.
  • Count falls below 500 per mm3 is an indication of disease progression and the need for antiretroviral therapy.
  • Counts below 200 denote risk of serious infections.
  1. Direct Measurement of HIV RNA

Necessary in the course of treatment.

Done by two methods:

  • The reverse transcriptase PCR (RT-PCR) assay
  • The branched DNA (bDNA) assay.
  1. Beta-2-Microglobulin and Neopterin
  • These two substances which have a predictive value on the progression of HIV disease.
  • Can be measured in serum or urine.
  • Concentrations are low in asymptomatic infection and rise with advancing disease.

When HIV passes to a fetus or baby from an HIV positive mother, this is called vertical transmission.

When HIV passes between sexual partners or people who share needles, this is called horizontal transmission.

  • Effective management of HIV infection is possible using different combinations of available drugs.
  • This method of treatment is collectively known as antiretroviral therapy (ART).
  • Standard ART is comprised of a concoction of at least three medicines (termed as “highly active antiretroviral therapy” or HAART).
  • HAART is the acronym for “highly active antiretroviral therapy,” a term coined in the late 1990s to describe the effectiveness of combination drug therapies used to treat HIV.
  • In 1995, a combination drug treatment known as the “AIDS cocktail” was introduced.
  • This type of therapy is now known as highly active antiretroviral therapy (HAART).
  • It’s also called combination antiretroviral therapy (cART) or simply antiretroviral therapy (ART).
  • Control the multiplication of HIV.
  • Increases the count of CD4 cells, thus, prolonging the asymptomatic phase of infection, slowing the progression of the disease.
  • Helps in reducing the risk of transmission.
  • Reverse Transcriptase Inhibitors.
  • Protease Inhibitors.
  • Fusion Inhibitors.
  • Chemokine Receptor 5 Antagonist.
  • Integrase Strand Transfer Inhibitors.

• It a group of drugs, which can bind and inhibit the reverse transcriptase enzyme to intercept the multiplication of HIV.
• There are two types of inhibitors:
A. Non-nucleoside reverse transcriptase inhibitors (NNRTIs).
B. Nucleoside reverse transcriptase inhibitors (NRTI). E.g.:
• Zidovudine.
• Didanosine.
• Abacavir
• Tenofovir.
• Combivir.

• It blocks the functioning of protease enzymes in acutely and chronically HIV-infected CD4 cells.
• Inhibition of HIV protease enzymes results in the liberation of immature and noninfectious viral particles.E.g.:
A. Lopinavir
B. Indinavir
C. Ritonavir.
D. Nelfinavir.
E. Amprenavir.

  • These drugs act by blocking HIV from entering the CD4 cells of infected patients.
  • They inhibit the fusion of HIV particles with the CD4 cells. E.g:Enfuvirtide.
  • It prevents the infection by blocking the chemokine receptor 5 (CCR5) antagonist receptor present on CD4 cells.
  • In the absence of vacant CCR5 receptors, HIV fails to gain entry and infect the cell. E.g: Maraviroc.

• It prevents the integration of viral DNA into the host genome of CD4 cells by an integrase enzyme.
• Blocking integrase prevents HIV from replicating. E.g
A. Raltegravir.
B. Elvitegravir.
C. Dolutegravir.

Treatment options recommended by the World Health Organization (WHO) are first, second, and third line treatment.

• Consists of two nucleoside reverse-transcriptase inhibitors (NRTIs) and one non-nucleoside reverse-transcriptase inhibitor (NNRTI) or an integrase inhibitor (INSTI).
• Tenofovir disoproxil fumarate (TDF) + lamivudine (3TC) or emtricitabine (FTC) + efavirenz (EFV) as a fixed dose for this type of ART.
When this drug combination is contraindicated or is unavailable:
1. Zidovudine(AZT) + 3TC + EFV,
2. AZT + 3TC + Nevirapine (NVP), or
3. TDF + 3TC (or FTC) + NVP is used.
Pregnant and breastfeeding patients: First-line ART in this subpopulation is comprised of a single daily dose of:
• TDF + 3TC (or FTC) + EFV
Alternative first-line regimens
• AZT + 3TC + EFV (or NVP)
• TDF + 3TC (or FTC) + NVP
Pediatric patients:
Patients below three years of age:
• Lopinavir/Ritonavir (LPV/r)-based treatment, even under NNRTI exposure. When LPV/r is not a viable option, NVP based treatment should be used.
• For infected children over age three, EFV is the ideal NNRTI while NVP has been identified as the second option.
• For infected children younger than three years , who develop TB while on the Lopinavir/Ritonavir (LPV/r)-based treatment, the NRTI regimen should be switched to abacavir (ABC) + 3TC or AZT + 3TC until the TB infection is cleared.

Adults, including pregnant and breastfeeding patients:

  • When a first-line treatment of ART fails, a second-line ART should be utilized.
  • Comprised primarily of two NRTIs and a ritonavir-boosted PI.
  • The recommended option for second-line ART includes AZT and 3TC as the NRTI.
  • After the failure of AZT or stavudine (d4T) + 3TC-based first-line regimen, TDF + 3TC (or FTC) as the NRTI should be considered.
  • When first-line NNRTI-based treatment fails, two NRTIs + a boosted protease inhibitor (PI )are suggested.

Pediatric patients:

  • If first-line ART fails in children ages three and up, a second-line treatment consisting of one NNRTI and two NRTIs should be given.
  • If abacavir (ABC) or TDF + 3TC (or FTC) fails, the recommended option is AZT + 3TC.
  • After a failure of AZT or d4T + 3TC (or FTC) in first-line treatment, the preferred NRTI option is ABC or TDF + 3TC (or FTC).

If first- and second-line ART fails, the WHO recommends inclusion of new medicines with the least amount of risk for development of cross-resistance towards previously used drugs (e.g. integrase inhibitors and second-generation NNRTIs and PIs).

A. Gastrointestinal: Nausea, diarrhea, vomiting, taste perversion, constipation, dyspepsia, abdominal pain, hepatotoxicity, and pancreatitis.
B. Central nervous system: Headache, vision problems, dizziness, tinnitus, insomnia, paresthesia, pain/numbness/tingling in extremities, peripheral neuropathy, somnolence, excessive sleep at night, memory problems, loss of olfactory function, and hearing impairment.
C. Hematological: Anemia, bilirubinemia, increased urate, and blood in the urine.
D. Psychological: Anxiety, confusion, depression, nightmares, elation, and delusions.
E. Metabolic: Abnormal fat distribution (lipodystrophy), anorexia, dyspnea, fatigue, lethargy, and weight gain.
F. Dermatological: Skin rash, facial discoloration, and pruritus.
G. Musculoskeletal: Body aches and vague chest pain.
H. Miscellaneous: Hypersensitive reactions, oral ulcerations, fever, and irregular menstrual cycles.

  • The term “viral hepatitis” is usually applied to the acute stage of the disease which is characterized by fever, malaise, and jaundice, but seldom causes death.
  • Chronic manifestations are classified either as chronic hepatitis or massive liver necrosis.
  • In mild forms of the disease, the patient has flu-like symptoms of nausea and vomiting and a smoker may develop distaste for cigarettes.

Infectious hepatitis (hepatitis A)

  • Classified as hepatovirus, is a small, unenveloped symmetrical RNA virus.
  • Acquired orally.
  • Short incubation period of about 50 days
  • Occur primarily in children and young adults, sporadically and in epidemics.
  • The course runs from 6 to 8 weeks and the disease normally resolves with no sequelae.

Serum hepatitis (hepatitis B)

  • Hepatitis B virus (HBV), a member of the hepadnavirus group, double-stranded DNA viruses which replicate, unusually, by reverse transcription. 
  • Transmitted parenterally.
  • Incubation period of 50–100 days.
  • It occurs sporadically in any age group, but older individuals are more affected.


Hepatitis C virus

  • Hepatits C virus is a RNA virus belonging to family Flaviviridae.
  • Genetically distinct viral groups have evolved with 9 different genotypes of hepatitis C and 40 different subgroups
  • Incubation period is variable, ranging from 3 to 20 weeks, with a mean of 7 weeks.
  • Infected individuals have a transient alanine aminotransferase (ALT) level elevated greater than tenfold before the symptoms develop.
  • HCV is associated with chronic liver disease and with primary liver cancer.


Hepatitis D virus (HDV)

  • Unusual, single-stranded, circular RNA virus which has no independent existence.
  • It requires HBV for replication and has the same sources and modes of spread as HBV.
  • It can infect simultaneously with HBV or it can superinfect those who are already chronic carriers of HBV.
  • Thus, prevention of HDV infection is similar to prevention for HBV and relies strongly on HBV vaccination.

Hepatitis E virus (HEV)

  • RNA virus is excreted in the stools and spreads by the faeco–oral route.
  • The clinical illness resembles acute Hepatitis A virus (HAV) infection and recovery is the rule.
  • Chronic infection does not occur.

Hepatitis G virus (HGV)

  • Is an RNA virus that rarely occurs as a solitary infection and usually appears as a co-infection with hepatitis A, B, or C.
  • Transmitted through the blood and frequently associated with transfusions.
  • HBV and HCV infections are serious public health problems that can have consequences in terms of psychological and occupational diseases.
  • HBV and HCV are common causes of occupational diseases transmitted from patients to health care workers (HCWs) and vice versa.

• Blood transfusion.
• Percutaneous exposure through contaminated instruments.
• Occupational exposure to blood.
• Sexual contact.
• Perinatal and idiopathic routes.

Individuals at the greatest risk are:

  • Hemophiliacs.
  • Patients on dialysis.
  • Parenteral drug abusers.


Hepatitis B virus

Hepatitis C virus







Mode of transmission

Parentral, sexual, perinatal, oral fluids

Parentral, sexual, may get transmitted by oral fluids

Antigens in blood

HbsAg, HbeAg


Antibodies in blood

Anti-HBs, Anti-Hbe, Anti-HBc



Can be mild, severe, acute or chronic. Less than 5% of adult HBV infections become chronic

Hepatitis C is likely to become a chronic condition in 70 to 80% of infected people, with 10% developing severe liver disease

Passive immunization

Hepatitis B immune globulin

Not available

Active immunization

Recombivax, Engerix and Twinrix

Not available


DNA – De-oxyribonucleic acid; RNA – Ribonucleic acid; HCV – Hepatitis C virus; HBsAg – Hepatits B surface antigen; HBeAg – Hepatitis B e antigen; HBV – Hepatitis B virus.

Early symptoms occur before jaundice:

  • Malaise
  • Fatigue
  • Anorexia for a period of 1-2 weeks.

In the acute phase:

  • Nausea.
  • Vomiting.
  • Abdominal pain.
  • Jaundice.
  • Skin rashes.
  • Joint pain.
  • Arthritis.
  • Acute hepatitis B progresses to chronic HBV infection.
  • Chronic infection with HBV results in chronic liver disease, including liver cirrhosis and hepatocellular carcinoma.

Onset of hepatitis C infection is unrecognized because the clinical symptoms are often mild and clinically not apparent.

In symptomatic cases:

  • Malaise.
  • Nausea.
  • Vomiting.
  • Abdominal discomfort.
  • Pale stools.
  • Dark urine.
  • Jaundice.
  • Between 70% and 80% develop chronic infections that defined as infection persisting for more than 6 months with some evidence of hepatitis.


Hepatitis C infection leads to:

  • Mild hepatitis to cirrhosis.
  • Liver cancer.
  • Liver failure.

Manifestations in the oral cavity include:

  • Lichen planus.
  • Sjögrens syndrome.
  • Sialadenitis.
  • Some forms of oral cancers.
  • Cirrhotic patients have thrombocytopenia due to hypersplenism or treatment with interferon.
  • Petechiaes or excessive gingival bleeding with minor trauma.
  • Severe hemorrhage can ensue as a result of the paucity of clotting factors.
  • Increased prevalence of diabetes(due to the severity of liver disease or to the treatment with interferon).
  • HCV may act as an independent diabetogenic factor.
  • Diabetes associatedchanges like frequency of periodontal disease, stomatitis, candidiasis, cheilitis, oral leukoplakia, and dental caries.
  • HBs Ag positivity may induce or cause proneness to OLP and pitted keratolysis.
  • Drugs and interferons used for the treatment of hepatitis C also precipitate OLP.
  • HCV acts locally, altering the function of the epithelial cells, or that the immune response of the host to HCV is responsible for the development of OLP.
  • Salivary gland disorders associated with HCV are xerostomia, Sjögren’s syndrome, and sialadenitis.
  • Xerostomia increases susceptibility to caries and oral soft tissue disorders.
  • HCV causes sialadenitis associated with xerostomia.
  • Decrease in salivary flow may lead to dry mouth (particularly at night), halitosis, dental decay, and difficulty in talking, eating, and swallowing.


Sjögren’s syndrome

Hepatitis C virus

Sicca symptoms

Commonly present

Usually absent or modest

Parotid swelling

Moderate to severe

Mild to moderate

Extra-glandular manifestations

Mainly pulmonary, gastrointestinal, renal, and neurologic involvement

Mainly gastrointestinal and musculo-skeletal involvement


Periductal lymphocytic infiltration

Pericapillary lymphocytic infiltration

Infiltrating lymphocytic


Predominantly CD4+ T cells

Mixed CD4+ /CD8+ T cells


High-frequency RF, ANA, anti-Ro/SSA and anti-La/SSB, alpha-fodrin antibodies

High frequency of RF, ANA, alpha-fodrin, low prevalence of anti-Ro/SSA and anti-La/SSB antibodies, high frequency of cryoglobulins

HLA association

B8, DR2 and DR3



Preferentially affecting salivary glands

Affecting both liver and salivary glands

  • Dental health care provider should receive three doses of hepatitis B vaccination.
  • Describe the type of blood exposures that may place dental health care personnel (DHCP) at risk of infection.
  • Outline the procedures for promptly reporting and evaluating such exposures.
  • Identify the health care professional who is qualified to provide counseling and perform all medical evaluations and procedures in accordance with the most current US Public Health Care Service (CDC) recommendations.
  • Resource should be available that permits rapid access of exposed DHCP to clinical care, testing, counseling, and post-exposure prophylaxis (PEP) and the testing and counseling of source patients.

Exposure that might place a dentist at risk of hepatitis infection includes the following:

  • Percutaneous injuries (needlestick or cut with a sharp object).
  • Contact with potentially infectious blood, tissues, or other body fluids.
  • Mucus membranes of the eye, nose, or mouth or non-intact skin (exposed skin that is chapped, abraded, or afflicted with dermatitis).
  • Any blood or body fluid exposure to an unvaccinated person should lead to the initiation of the hepatitis B vaccine series (Recombivax HB® 10 mcg or Energix‑B® 20 mcg IM at 0, 1, and 6 months).
  • When hepatitis B Immune Globulin (HBIG) is indicated, it should be administered as soon as possible after the exposure (preferable within 24 h, but it is recommended up to 1 week following an occupational exposure).
  • Hepatitis B vaccine can be administered simultaneously with HBIG but at a separate site.
  • Test for anti‑HBs must be performed 1-2 months after the last dose of vaccine.
  • Anti‑HBs cannot be ascertained if HBIG has been administered within the previous 6 weeks.
  • On exposure to HCV, test for anti‑HCV must be carried out for the source.
  • Baseline testing for anti‑HCV and Alanine aminotransferase activity (ALT) should be carried out.
  • Recent assays are based on RT‑PCR that can detect minute amounts of HCV RNA (down to 10 international units (IU)/ml) and accurately quantify HCV RNA levels up to approximately 107 IU/ml.

Follow‑up testing for anti‑HCV and ALT activity and HCV RNA by PCR at 4-6 weeks must be carried out forearly detection.


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