Quick Answer
DNA viruses are a compact NEET PG microbiology chapter — only seven families cause almost all human DNA-virus disease, and the same MCQ patterns recur every year at INI-CET and AIIMS. Master these six anchors.
- Herpesviridae (double-stranded DNA, enveloped, icosahedral) — 8 HHVs. HSV-1 (oral, encephalitis), HSV-2 (genital), VZV (chickenpox, zoster), EBV (mono, Burkitt), CMV (mono-like, congenital, transplant), HHV-6/7 (roseola), HHV-8 (Kaposi).
- Papillomaviridae — HPV; low-risk 6/11 warts, high-risk 16/18 cervical + anal + oropharyngeal SCC via E6-p53 and E7-RB inactivation.
- Hepadnaviridae — HBV; partially double-stranded circular DNA with reverse transcriptase; chronic HBV drives cirrhosis and HCC.
- Adenoviridae — respiratory, conjunctivitis, gastroenteritis, haemorrhagic cystitis; used as vaccine vector.
- Parvoviridae — B19; fifth disease, aplastic crisis in sickle cell, hydrops fetalis.
- Polyomaviridae (BK, JC) and Poxviridae (molluscum, smallpox — eradicated 1980, monkeypox re-emerging).
DNA viruses cause a disproportionate share of NEET PG microbiology marks because they include the herpes group (recurrent latent-reactivation stems), HPV (India's cervical cancer story), HBV (chronic hepatitis and HCC) and parvovirus B19 (sickle cell aplastic crisis and hydrops fetalis). Examiners love pairing an inclusion body, a serology panel or a vector-hosted disease with an India-specific twist.
This NEETPGAI deep dive walks through all seven DNA virus families, the eight human herpesviruses, HBV serology interpretation, HPV oncogenesis, congenital CMV and the classical inclusion bodies — with the India-specific context (birth-dose HBV vaccine, Cervavac roll-out, sickle cell parvovirus crisis in tribal belts) examiners test. Pair it with the parasitology tropical infections guide for the broader vector-borne microbiology coverage.
DNA virus families — the seven you need to know
All DNA viruses replicate in the nucleus (with one exception — poxvirus, which replicates in the cytoplasm because it carries its own DNA polymerase). Six are double-stranded DNA; parvovirus is uniquely single-stranded.
| Family | Genome | Envelope | Key human pathogens |
|---|
| Herpesviridae | dsDNA linear | Enveloped | HSV-1, HSV-2, VZV, EBV, CMV, HHV-6, HHV-7, HHV-8 |
| Papillomaviridae | dsDNA circular | Non-enveloped | HPV (over 200 types) |
| Polyomaviridae | dsDNA circular | Non-enveloped | BK virus, JC virus, Merkel cell polyomavirus |
| Adenoviridae | dsDNA linear | Non-enveloped | Adenovirus (over 50 serotypes) |
| Hepadnaviridae | Partially dsDNA circular; uses reverse transcriptase | Enveloped | Hepatitis B virus |
| Parvoviridae | ssDNA linear | Non-enveloped | Parvovirus B19 |
| Poxviridae | dsDNA linear; replicates in cytoplasm | Enveloped (complex) | Variola (smallpox — eradicated), vaccinia, molluscum contagiosum, monkeypox |
Mnemonic — DNA viruses that are non-enveloped are Papovaviridae (Papilloma, Polyoma), Adenoviridae, Parvoviridae — mnemonic PAP.
Herpesviridae — the big eight
All herpesviruses share three features — dsDNA, enveloped icosahedral capsid, and lifelong latency with periodic reactivation. Latency location and reactivation trigger vary by virus.
HSV-1 and HSV-2
- Transmission — direct contact with lesions or secretions. HSV-1 predominantly oro-labial (though rising as genital cause in the West), HSV-2 predominantly genital.
- Latency — HSV-1 in trigeminal ganglion; HSV-2 in sacral dorsal root ganglia.
- Clinical — HSV-1 herpes labialis, herpes gladiatorum, herpetic whitlow, keratitis (dendritic ulcer on fluorescein), Bell palsy (some cases), and the feared temporal-lobe haemorrhagic encephalitis (most common sporadic viral encephalitis).
- HSV-2 — recurrent genital ulcers with prodrome, and neonatal HSV (disseminated, encephalitis, mucocutaneous) from vertical transmission via birth canal.
- Diagnosis — Tzanck smear (multinucleated giant cells, not specific), viral culture, PCR (most sensitive, gold standard for encephalitis on CSF), Cowdry type A inclusions on histology.
- Treatment — acyclovir (oral for uncomplicated genital; IV for encephalitis and neonates), valacyclovir, famciclovir. Suppressive therapy for frequent recurrences.
VZV (HHV-3)
- Primary infection — varicella (chickenpox) — dew-drop-on-a-rose-petal vesicles in different stages of evolution (unlike smallpox where all lesions are same stage).
- Reactivation — herpes zoster (shingles) — dermatomal vesicular eruption. Ramsay Hunt syndrome is zoster of the geniculate ganglion — facial palsy plus ear vesicles plus loss of taste on anterior two-thirds of tongue.
- Complications — postherpetic neuralgia (main long-term issue), disseminated zoster in immunocompromised, ophthalmic zoster with Hutchinson sign (nasociliary branch, tip of nose vesicles — corneal involvement risk).
- Vaccine — live-attenuated varicella vaccine (childhood); recombinant zoster vaccine (Shingrix) for older adults, superior to the older live-attenuated Zostavax.
- Treatment — acyclovir, valacyclovir, famciclovir. Start within 72 hours of rash for best outcome.
EBV (HHV-4)
- Latency — memory B cells.
- Clinical — infectious mononucleosis (fever, exudative pharyngitis, cervical lymphadenopathy, splenomegaly, hepatitis). Downey cells are atypical reactive T lymphocytes on peripheral smear. Heterophile antibody Monospot is positive in most adults but often negative in young children.
- Trap — do NOT give ampicillin or amoxicillin during EBV mono — produces a widespread maculopapular rash (non-allergic).
- Malignancies — Burkitt lymphoma (endemic African jaw form, EBV strongly linked; sporadic form less so), nasopharyngeal carcinoma (Southeast Asian, Chinese), Hodgkin lymphoma (mixed cellularity in HIV), post-transplant lymphoproliferative disease (PTLD), primary CNS lymphoma in AIDS, oral hairy leukoplakia (HIV).
- Diagnosis — heterophile antibody, EBV-specific serology (VCA-IgM for acute), EBV PCR for tissue.
CMV (HHV-5)
- Latency — monocytes, dendritic cells, CD34 progenitors.
- Clinical — heterophile-negative mononucleosis-like syndrome in healthy adults. Serious disease in immunocompromised — retinitis (pizza-pie fundus in AIDS), colitis, oesophagitis, pneumonitis, hepatitis, encephalitis. Transplant recipients — CMV disease within first 100 days is a major cause of morbidity.
- Congenital CMV — commonest congenital viral infection; periventricular calcifications, sensorineural hearing loss (leading non-genetic cause), microcephaly, chorioretinitis, hepatosplenomegaly, thrombocytopenic purpura (blueberry muffin baby).
- Histology — giant infected cell with intranuclear owl-eye inclusion.
- Treatment — ganciclovir, valganciclovir (oral prodrug), foscarnet, cidofovir (nephrotoxic), letermovir (prophylaxis in stem cell transplant).
HHV-6 and HHV-7
Cause roseola infantum (exanthem subitum, sixth disease) — high fever for 3 to 5 days that abruptly resolves as a rose-pink maculopapular rash appears on the trunk. Febrile seizures common during the pyrexial phase. HHV-6 also reactivates in transplant recipients.
HHV-8
Kaposi sarcoma-associated herpesvirus. Causes Kaposi sarcoma in AIDS (violaceous plaques on skin, oral mucosa, visceral), primary effusion lymphoma and multicentric Castleman disease.
Papillomaviridae — HPV and cervical cancer
HPV is a small non-enveloped dsDNA virus with over 200 types. Low-risk types 6 and 11 cause anogenital warts (condyloma acuminatum) and juvenile recurrent respiratory papillomatosis (in babies of infected mothers). High-risk types 16 and 18 (also 31, 33, 45, 52, 58) cause cervical, anal, vulvar, penile and oropharyngeal squamous cell carcinoma.
HPV oncogenesis
Two viral proteins drive transformation:
- E6 binds and degrades p53 — removes apoptosis after DNA damage.
- E7 binds and inactivates RB — removes the G1/S cell cycle checkpoint.
Cervical cytology
- Koilocytes — squamous cells with raisin-like hyperchromatic nuclei and perinuclear haloes; pathognomonic for HPV infection.
- Cervical screening: Pap smear from age 21, HPV DNA testing from 30, or VIA (visual inspection with acetic acid) in low-resource Indian settings.
Vaccines
- Cervavac — India's own indigenous quadrivalent HPV vaccine (types 6, 11, 16, 18); rolled out under the Universal Immunisation Programme for girls aged 9 to 14 from 2024.
- Gardasil-9 — international 9-valent (adds 31, 33, 45, 52, 58).
- Vaccine is preventive, not therapeutic — best before sexual debut.
Hepadnaviridae — HBV
HBV is unique among DNA viruses in having a partially double-stranded circular DNA genome and using reverse transcriptase in its replication cycle. It infects hepatocytes via the NTCP (sodium taurocholate cotransporting polypeptide) receptor.
Serology decoded
| Marker | Meaning |
|---|
| HBsAg | Currently infected — acute or chronic |
| Anti-HBs | Immunity — vaccine or resolved infection |
| Anti-HBc IgM | Acute infection or window period |
| Anti-HBc IgG | Past or chronic infection (lifelong) |
| HBeAg | High replication and infectivity |
| Anti-HBe | Seroconversion; usually falling viral load |
| HBV DNA | Quantitative viral load |
Serology patterns:
- Acute HBV — HBsAg+, anti-HBc IgM+, HBeAg+.
- Chronic HBV — HBsAg+ more than 6 months, anti-HBc IgG+.
- Resolved infection — anti-HBs+, anti-HBc IgG+.
- Vaccinated — anti-HBs+ alone.
- Window period — anti-HBc IgM+ alone (HBsAg cleared, anti-HBs not yet appeared).
Clinical
- Acute — most adults recover; risk of chronic infection higher with earlier acquisition (90 percent in perinatal transmission, 5 to 10 percent in adult).
- Chronic HBV — cirrhosis, hepatocellular carcinoma. India has an estimated 40 million HBV carriers.
- Extra-hepatic — polyarteritis nodosa (immune-complex vasculitis), membranous nephropathy, membranoproliferative GN.
Treatment and prevention
- Antivirals — tenofovir, entecavir (first line for chronic HBV); pegylated interferon in select cases.
- Universal Immunisation Programme birth-dose HBV vaccine in India within 24 hours of birth, plus subsequent doses at 6, 10 and 14 weeks. Highly effective at preventing perinatal transmission.
- Passive immunisation with HBIG plus vaccine for perinatal exposure and needlestick injury.
Other DNA viruses worth knowing
Adenoviridae
- Respiratory illness (children and military recruits), pharyngoconjunctival fever, epidemic keratoconjunctivitis (swimming pool conjunctivitis), gastroenteritis (types 40, 41), haemorrhagic cystitis (post-transplant).
- Used as vaccine vector (Oxford-AstraZeneca COVID-19 vaccine ChAdOx1, Sputnik V, Ad26).
Polyomaviridae
- BK virus — post-renal-transplant nephropathy, haemorrhagic cystitis after bone marrow transplant.
- JC virus — progressive multifocal leukoencephalopathy (PML) in AIDS and in multiple sclerosis patients on natalizumab; look for anti-JCV antibody screening before starting natalizumab.
- Merkel cell polyomavirus — Merkel cell carcinoma (aggressive neuroendocrine skin cancer).
Parvoviridae — B19
- Single-stranded DNA. Targets erythroid progenitors via the P antigen receptor on red cell precursors.
- Fifth disease (erythema infectiosum) — "slapped-cheek" rash in children.
- Aplastic crisis — in chronic haemolytic anaemia (sickle cell, hereditary spherocytosis, thalassaemia) — B19 arrests red cell production and haemoglobin drops abruptly. Major issue in Indian tribal-belt sickle cell.
- Hydrops fetalis — vertical transmission in pregnancy causing severe fetal anaemia and non-immune hydrops.
- Polyarthritis in adults, particularly women.
- Pure red cell aplasia in immunocompromised.
Poxviridae
- Smallpox (variola) — eradicated in 1980 through WHO global campaign; last natural case 1977 in Somalia. Vesicles all in the same stage of evolution (contrasts with chickenpox).
- Vaccinia — the vaccine strain historically used.
- Molluscum contagiosum — umbilicated pearly papules on skin; direct contact; self-limiting but can be persistent in HIV. Molluscum bodies (Henderson-Paterson bodies) on histology.
- Monkeypox (mpox) — re-emerging zoonosis; 2022 to 2023 global outbreak among MSM communities; central African clade more virulent than West African clade.
Diagnostic inclusion bodies at a glance
| Inclusion body | Virus |
|---|
| Cowdry type A intranuclear | HSV, VZV |
| Cowdry type B intranuclear | Poliovirus, adenovirus |
| Owl-eye intranuclear | CMV |
| Molluscum (Henderson-Paterson) intracytoplasmic | Molluscum contagiosum |
| Guarnieri intracytoplasmic | Smallpox, vaccinia |
| Negri intracytoplasmic (Purkinje, hippocampus) | Rabies (an RNA virus, but tested here) |
| Councilman body (apoptotic hepatocyte) | Yellow fever |
| Amphophilic intranuclear in koilocytes | HPV |
India-specific and NEET PG traps
- Temporal lobe haemorrhagic encephalitis — HSV-1; treat empirically with IV acyclovir at the first suspicion; delay costs lives.
- HSV keratitis — dendritic ulcer on fluorescein; topical acyclovir; do NOT give topical steroids (perforation risk).
- Neonatal HSV — high mortality; IV acyclovir; caesarean if active maternal genital lesions.
- Ramsay Hunt syndrome — VZV facial palsy with ear vesicles; corticosteroid plus acyclovir.
- Ampicillin rash in EBV mono — classic trap; do not label as penicillin allergy.
- Burkitt lymphoma — starry-sky histology, t(8;14) MYC translocation, jaw mass in African child.
- CMV retinitis — pizza-pie fundus in AIDS with CD4 less than 50; ganciclovir.
- Congenital CMV vs toxoplasmosis calcifications — CMV periventricular, toxoplasmosis scattered.
- Roseola infantum — HHV-6/7; abrupt defervescence as rash appears; febrile seizure common.
- Kaposi sarcoma — HHV-8; palate and hard palate lesions in HIV; treat with ART primarily.
- HPV E6-p53 and E7-RB — the molecular basis of cervical carcinogenesis.
- Koilocytes — HPV signature on cervical cytology.
- Cervavac — India's indigenous quadrivalent HPV vaccine.
- HBV birth-dose vaccine — within 24 hours in India UIP; prevents perinatal transmission.
- HBV window period — anti-HBc IgM alone; classical MCQ.
- HBV chronic — HBsAg positive more than 6 months.
- HBV extra-hepatic — polyarteritis nodosa, membranous nephropathy.
- Parvovirus B19 in sickle cell — aplastic crisis; India tribal-belt relevance.
- B19 in pregnancy — hydrops fetalis; ultrasound surveillance.
- JC virus PML — natalizumab warning; anti-JCV antibody screening before use.
- Molluscum contagiosum in HIV — extensive facial lesions; treat with cryotherapy or curettage; consider HIV testing.
- Monkeypox — re-emerging; look for lymphadenopathy which distinguishes from smallpox; PCR confirmation.
Frequently asked questions
Which viruses belong to the herpesvirus family and where does each stay latent?
There are eight human herpesviruses. HSV-1 (HHV-1) is latent in the trigeminal ganglion and reactivates as cold sores or (rarely) temporal-lobe haemorrhagic encephalitis. HSV-2 (HHV-2) is latent in sacral dorsal root ganglia and reactivates as genital herpes; it is a leading neonatal encephalitis cause via birth canal exposure. VZV (HHV-3) is latent in dorsal root ganglia and reactivates as herpes zoster — Ramsay Hunt syndrome is zoster of the geniculate ganglion with facial palsy and ear vesicles. EBV (HHV-4) is latent in memory B cells and drives infectious mononucleosis, Burkitt lymphoma, nasopharyngeal carcinoma and Hodgkin lymphoma. CMV (HHV-5) is latent in monocytes and CD34 progenitors and reactivates in transplant recipients as retinitis or colitis. HHV-6 and HHV-7 cause roseola infantum. HHV-8 is oncogenic and causes Kaposi sarcoma in HIV.
How do you interpret the hepatitis B serology panel?
HBsAg positive means the person has HBV — acute or chronic. Anti-HBs alone means immunity from vaccination or resolved infection. Anti-HBc IgM appears in acute infection and the window period when HBsAg has cleared but anti-HBs has not appeared. Anti-HBc IgG persists lifelong in past infection (with anti-HBs) or in chronic infection (with HBsAg still positive). HBeAg indicates high replication and infectivity. Anti-HBe indicates seroconversion, usually with falling viral load. HBV DNA quantifies active replication. Classical patterns — acute HBV: HBsAg positive, anti-HBc IgM positive, HBeAg positive. Chronic HBV: HBsAg positive more than 6 months, anti-HBc IgG positive. Resolved HBV: anti-HBs and anti-HBc IgG positive. Vaccinated: anti-HBs positive only. Window period: anti-HBc IgM positive only.
What are the classical viral inclusion bodies and which viruses cause them?
Cowdry type A intranuclear inclusion body — HSV and VZV (eosinophilic, surrounded by clear halo, one per nucleus). Cowdry type B — poliovirus and adenovirus. Owl-eye intranuclear inclusion body — CMV (giant infected cells with a large basophilic inclusion surrounded by halo). Molluscum bodies (Henderson-Paterson bodies) — molluscum contagiosum (large intracytoplasmic eosinophilic inclusions filling infected keratinocytes). Guarnieri bodies — smallpox (variola) and vaccinia (intracytoplasmic). Negri bodies — rabies virus (intracytoplasmic eosinophilic in Purkinje and hippocampal neurons; classic even though rabies is an RNA virus). Councilman bodies — yellow fever (apoptotic hepatocytes). Amphophilic intranuclear inclusions in koilocytes — HPV in cervical cytology.
Which HPV types cause cancer and which cause warts?
Low-risk HPV types 6 and 11 cause anogenital warts (condyloma acuminatum) and juvenile recurrent respiratory papillomatosis. High-risk HPV types 16, 18, 31, 33, 45, 52 and 58 cause cervical, anal, vulvar, penile and oropharyngeal squamous cell carcinoma. HPV 16 and 18 alone account for about 70 percent of cervical cancer globally. Oncogenesis is driven by two viral proteins: E6 binds and degrades p53 (removes apoptosis after DNA damage) and E7 binds and inactivates the RB tumor suppressor (removes G1/S checkpoint). Cervical cytology koilocytes — raisin-like nuclei with perinuclear haloes — are the pathognomonic HPV-infected cells. The Indian quadrivalent Cervavac (types 6, 11, 16, 18) and the international 9-valent Gardasil-9 (adds 31, 33, 45, 52, 58) are both used; India rolled out national HPV vaccination in girls aged 9 to 14.
What is the presentation and treatment of congenital CMV infection?
Congenital cytomegalovirus is the leading non-genetic cause of sensorineural hearing loss in India and worldwide. It is acquired transplacentally during maternal primary infection or reactivation. About 10 percent of infected newborns are symptomatic at birth — periventricular calcifications (contrast with toxoplasmosis which produces scattered intracranial calcifications), sensorineural hearing loss, microcephaly, chorioretinitis, hepatosplenomegaly, thrombocytopenic petechiae (blueberry muffin rash), jaundice and intrauterine growth restriction. The classical pathology finding is the giant infected cell with a large basophilic intranuclear owl-eye inclusion. Diagnosis is by urine or saliva CMV PCR within the first 3 weeks of life. Treatment for symptomatic congenital CMV is oral valganciclovir or IV ganciclovir for 6 months to reduce sensorineural hearing loss and improve developmental outcomes.
This content is for educational purposes for NEET PG exam preparation. It is not a substitute for professional medical advice, diagnosis, or treatment. Clinical information has been reviewed by qualified medical professionals.
Written by: NEETPGAI Editorial Team
Reviewed by: Pending SME Review
Last reviewed: September 2026
