Poliovirus & Enteroviruses

The Enterovirus genus (family Picornaviridae) is a recurring NEET PG favourite that bridges Microbiology, Medicine, Paediatrics and Community Medicine. This note covers poliovirus serotypes, the OPV-versus-IPV debate, VAPP/VDPV, anterior horn cell pathology, and the non-polio enteroviruses (Coxsackie A & B, Echovirus, EV-71, EV-D68) along with the global eradication endgame.

Classification: the Picornavirus family

Picornaviruses are small (pico) RNA viruses — non-enveloped, icosahedral, positive-sense single-stranded RNA, replicating in the cytoplasm. The genus Enterovirus is acid-stable (survives gastric pH), which is why these are faeco-orally transmitted enteric viruses, in contrast to the acid-labile Rhinovirus.

Genus (Picornaviridae)	Acid stability	Optimum temp	Key members
Enterovirus	Acid-stable (pH 3–9)	37°C	Poliovirus 1–3, Coxsackie A & B, Echovirus, EV-68 to 71, Hepatitis A*
Rhinovirus	Acid-labile (destroyed <pH 6)	33°C (nasal mucosa)	>100 serotypes, common cold
Hepatovirus	Acid-stable	37°C	Hepatitis A virus
Aphthovirus	Acid-labile	—	Foot-and-mouth disease (cattle)

High-yield: Enteroviruses are acid-stable and ether-resistant (non-enveloped). Rhinovirus is acid-labile and grows best at 33°C, matching the cooler nasal passages. The "enteric vs respiratory" temperature distinction is a classic one-liner.

The traditional split was Polio (3 types), Coxsackie A (≈23 types), Coxsackie B (6 types), and Echovirus (≈28 types). Modern taxonomy reclassifies them into Enterovirus species A–D by genome, but exams still test the old clinical names.

Structure & antigenic make-up

• Capsid: 60 copies each of four proteins — VP1, VP2, VP3, VP4. VP1, VP2, VP3 are surface-exposed and carry neutralising epitopes; VP4 is internal, anchoring RNA to the capsid.
• Receptors: Poliovirus uses CD155 (PVR / poliovirus receptor); Coxsackie B and adenovirus share the CAR (coxsackie-adenovirus receptor); EV-71 uses SCARB2.
• Genome: ~7.4 kb (+)ssRNA acting directly as mRNA; translated into a single polyprotein cleaved by viral proteases (2A, 3C). A VPg protein is covalently linked to the 5′ end.

High-yield: Poliovirus receptor = CD155 (PVR). Coxsackie B receptor = CAR, shared with adenovirus. VP1 carries the major neutralising antigenic site and is used for genotyping/serotyping.

Poliovirus

Serotypes and significance

Three serotypes — PV1, PV2, PV3 — with no cross-protection, so a trivalent vaccine was historically needed.

• Wild poliovirus type 2 (WPV2): eradicated, certified 2015.
• Wild poliovirus type 3 (WPV3): eradicated, certified 2019.
• Wild poliovirus type 1 (WPV1): the only wild strain still circulating, endemic in Pakistan and Afghanistan.

Pathophysiology — the journey to the anterior horn

The virus is ingested → replicates in the oropharyngeal and intestinal lymphoid tissue (tonsils, Peyer's patches) → minor viraemia seeds the reticuloendothelial system → major viraemia → in <1% it crosses into the CNS and selectively destroys anterior (ventral) horn motor neurons of the spinal cord (and motor nuclei of the brainstem in bulbar disease).

Stepwise spread: Ingestion → gut/pharyngeal lymphoid replication → minor (primary) viraemia → major (secondary) viraemia → CNS invasion → anterior horn cell necrosis → flaccid paralysis.

High-yield: Polio causes asymmetric, flaccid, areflexic, pure-motor LMN paralysis with intact sensation. The lesion is the anterior horn cell. This sensory sparing distinguishes it from Guillain–Barré syndrome.

Clinical spectrum

Outcome	Approx. frequency	Features
Inapparent / asymptomatic	~90–95%	Subclinical, immunising
Abortive polio (minor illness)	~4–8%	Fever, sore throat, malaise, GI upset; non-specific
Non-paralytic (aseptic meningitis)	1–2%	Meningism, lymphocytic CSF, full recovery
Paralytic polio	<1% (≈0.1–0.5%)	Asymmetric flaccid paralysis, legs > arms

Paralytic forms: spinal (most common, asymmetric limb weakness), bulbar (cranial nerve/respiratory centre — high mortality), and bulbospinal. Provocation paralysis — IM injections, tonsillectomy, or strenuous exercise during the viraemic phase localise paralysis to that limb.

Diagnosis

• Specimen of choice: two stool samples collected 24–48 h apart within 14 days of paralysis onset (virus shed for weeks). Throat swab is useful early; CSF yield is poor.
• Virus isolation in cell culture, then intratypic differentiation (ITD) by RT-PCR to separate wild, vaccine (Sabin) and vaccine-derived (VDPV) strains.
• Acute paralytic case → CSF shows raised cells (lymphocytic), normal/slightly raised protein, normal glucose (aseptic meningitis picture).

High-yield: Investigation of choice for confirming polio = viral isolation from two stool samples, then genomic sequencing/ITD. Serology (rising antibody titre) is supportive but cannot distinguish wild from vaccine virus.

OPV versus IPV — the most-tested table

Feature	OPV (Sabin)	IPV (Salk)
Nature	Live attenuated	Killed (formalin-inactivated)
Route	Oral	Intramuscular / subcutaneous
Immunity	Humoral (IgG) + intestinal mucosal IgA	Mainly humoral IgG, poor gut immunity
Herd / community immunity	Yes (faeco-oral spread of vaccine virus)	No
Reversion to virulence	Yes → VAPP / VDPV	None (cannot revert)
Use in immunocompromised	Contraindicated	Safe / preferred
Cold chain	Strict (heat-labile)	More stable
Cost / ease	Cheap, easy, no needle	Costlier, needs trained staff
Developed by	Albert Sabin	Jonas Salk

High-yield: OPV gives intestinal mucosal (secretory IgA) immunity and herd immunity but can revert → VAPP. IPV gives strong humoral immunity, no gut immunity, but is safe in the immunocompromised. This single contrast is asked almost every year.

VAPP and VDPV

• VAPP (Vaccine-Associated Paralytic Poliomyelitis): clinically identical paralysis caused by reversion of the attenuated vaccine virus, classically Sabin type 2 and type 3. Risk ≈ 1 in 2.4–2.7 million doses (highest with the first dose). Occurs in the vaccinee or a close contact.
• VDPV (Vaccine-Derived Poliovirus): vaccine virus that has circulated long enough in under-immunised populations to regain neurovirulence and transmissibility (cVDPV, mostly type 2). This is now the dominant cause of vaccine-related outbreaks.

High-yield: Because type 2 Sabin caused most VAPP/cVDPV2, the world switched from trivalent OPV (tOPV) → bivalent OPV (bOPV, types 1 & 3) in the global "Switch" of April 2016, with at least one dose of IPV added to cover type 2. nOPV2 (novel, genetically stabilised) is now used for cVDPV2 outbreaks.

Polio in the Indian programme

• India certified polio-free: 27 March 2014 (WHO South-East Asia Region). Last wild case: Rukhsar Khatun, West Bengal, 13 January 2011.
• Under the Universal Immunisation Programme: bOPV at birth, 6, 10, 14 weeks and a booster at 16–24 months, plus a fractional/full IPV dose (introduced 2015–16). Pulse Polio (National Immunisation Days) target all <5-year-olds.
• AFP (Acute Flaccid Paralysis) surveillance is the cornerstone: every child <15 yr with AFP is investigated with two stool samples; target non-polio AFP rate ≥1 per 100,000 children <15 yr (sensitivity indicator).

High-yield: Eradication endgame = stop all type-2 OPV → eventually replace OPV entirely with IPV-only schedule once wild and vaccine type-2 risk ends. Smallpox is eradicated; polio and dracunculiasis (Guinea worm) are the leading targeted for eradication diseases.

Coxsackieviruses

Named after Coxsackie, New York. Differentiated historically by suckling-mouse pathology: Group A → widespread flaccid (myositis) paralysis and death; Group B → focal/spastic paralysis with damage to brown fat, pancreas, myocardium.

Coxsackie A — clinical syndromes

• Herpangina: abrupt fever + vesicles/ulcers on the soft palate, uvula and anterior tonsillar pillars (posterior oropharynx). Caused mainly by Coxsackie A.
• Hand-Foot-and-Mouth Disease (HFMD): vesicular rash on palms, soles and oral mucosa in young children; mild and self-limiting. Classic agents Coxsackie A16 and Enterovirus 71.
• Acute haemorrhagic conjunctivitis: Coxsackie A24 and Enterovirus 70.

Coxsackie B — clinical syndromes

• Bornholm disease (epidemic pleurodynia / "devil's grip"): sudden fever with paroxysmal, severe pleuritic chest/abdominal muscle pain due to intercostal myositis.
• Myocarditis and pericarditis: Coxsackie B is the commonest viral cause of myocarditis and a major cause of dilated cardiomyopathy; in neonates it causes fulminant myocarditis.
• Aseptic meningitis and association with juvenile (type 1) diabetes mellitus (pancreatic islet tropism).

High-yield: Memorise the split — CoxsackieAhh, my throat! = A → above the diaphragm head/throat lesions (herpangina, HFMD); B → Body/heart (myocarditis, pleurodynia, pancreatitis). EV-71 causes severe HFMD with brainstem encephalitis and is the most neurovirulent non-polio enterovirus.

Echovirus and other enteroviruses

• Echovirus = Enteric Cytopathic Human Orphan virus (originally "orphan" = no known disease; ~28 serotypes). It is the single commonest cause of viral (aseptic) meningitis and also causes febrile rash illness, neonatal sepsis-like syndromes and summer diarrhoea.
• Enterovirus 70: acute haemorrhagic conjunctivitis.
• Enterovirus 71: severe HFMD + brainstem encephalitis, epidemics in the Asia–Pacific.
• Enterovirus D68: respiratory illness with outbreaks of acute flaccid myelitis (AFM) — a polio-like paralysis in children (longitudinal grey-matter cord lesions on MRI).

High-yield: Commonest cause of aseptic/viral meningitis = enteroviruses (Echovirus & Coxsackie B). Acute flaccid myelitis in a polio-free era is linked to EV-D68.

Aseptic meningitis CSF: enterovirus vs the differentials

Parameter	Viral (entero)	Pyogenic bacterial	Tuberculous
Cells	↑ Lymphocytes	↑↑ Neutrophils	↑ Lymphocytes
Protein	Normal/mildly ↑	Markedly ↑	Markedly ↑
Glucose	Normal	Very ↓	↓
Appearance	Clear	Turbid	Cobweb clot

High-yield: Enteroviral meningitis = lymphocytic pleocytosis with normal glucose and clear CSF; CSF PCR (RT-PCR) is now the diagnostic test of choice and far outperforms culture.

Management

There is no specific antiviral for polio or other enteroviruses — management is supportive.

• Polio: bed rest, analgesia, physiotherapy, hot packs; mechanical ventilation for bulbar/respiratory paralysis (historically the "iron lung"). Avoid IM injections during acute illness (provocation). Prevention = vaccination.
• Pleconaril (capsid-binding agent) has been trialled for severe neonatal enteroviral sepsis and meningoencephalitis but is not routinely available/approved.
• IVIG is used in neonatal enteroviral myocarditis/sepsis and in chronic enteroviral meningoencephalitis in agammaglobulinaemic patients.
• Myocarditis: supportive heart-failure management; avoid NSAIDs early.

High-yield: No licensed antiviral exists in routine practice — the drug-equivalent answer is the vaccine (OPV/IPV). Investigational antiviral = pleconaril.

Complications

• Polio: residual flaccid paralysis, limb deformity/shortening, scoliosis, respiratory failure (bulbar), and the post-polio syndrome — new weakness, fatigue and pain appearing decades after the acute illness due to motor-unit attrition.
• Coxsackie B: dilated cardiomyopathy, neonatal myocarditis (high mortality), chronic pancreatitis/diabetes association.
• EV-71/D68: brainstem encephalitis, neurogenic pulmonary oedema, acute flaccid myelitis with permanent weakness.

Key differentials of acute flaccid paralysis

Feature	Poliomyelitis	Guillain–Barré (AIDP)	Traumatic neuritis	Transverse myelitis
Onset	24–48 h, asymmetric	Days, symmetric ascending	After IM injection	Acute
Lesion	Anterior horn cell (LMN)	Peripheral nerve/root	Sciatic/peripheral nerve	Spinal cord
Sensory	Spared	Often paraesthesia	Pain present	Sensory level present
Reflexes	Absent (affected limb)	Globally absent	↓ affected limb	Variable; up later
CSF	Pleocytosis	Albuminocytological dissociation (↑protein, normal cells)	Normal	Variable
Recovery	Often incomplete	Usually good	Good	Variable

High-yield: Any child <15 yr with acute flaccid paralysis is a suspect polio case until proven otherwise and must trigger AFP surveillance with two stool samples — irrespective of the most likely clinical diagnosis (GBS, traumatic neuritis, etc.).

Recently asked / exam angle

• OPV vs IPV comparison (route, immunity type, herd immunity, safety in immunocompromised) — perennial 1–2 markers.
• Poliovirus receptor = CD155 (PVR); Coxsackie B/adenovirus = CAR.
• Cause of VAPP → reversion of Sabin type 2/3; reason for the tOPV→bOPV "Switch" (2016).
• Specimen for polio diagnosis = two stool samples within 14 days of onset.
• Coxsackie A → herpangina/HFMD; Coxsackie B → myocarditis, Bornholm disease, pancreatitis.
• Echovirus / enteroviruses = commonest cause of aseptic meningitis; CSF picture (lymphocytes, normal sugar).
• EV-71 = severe HFMD + encephalitis; EV-D68 = acute flaccid myelitis.
• India polio-free certification year (2014) and last wild case (2011, West Bengal) — Community Medicine crossover.
• Picornavirus capsid proteins VP1–4 (VP4 internal); acid-stable vs Rhinovirus acid-labile/33°C.
• Post-polio syndrome as a delayed complication; pleconaril as the investigational antiviral.

Rapid revision

1. Picornaviruses: small, non-enveloped, (+)ssRNA, cytoplasmic replication; enteroviruses are acid-stable, rhinovirus acid-labile/grows at 33°C.
2. Capsid = VP1, VP2, VP3 (surface, neutralising) + VP4 (internal).
3. Poliovirus receptor = CD155 (PVR); Coxsackie B = CAR; EV-71 = SCARB2.
4. Polio: **<1%** develop paralytic disease; lesion = **anterior horn cell**; **asymmetric flaccid pure-motor paralysis with intact sensation**, legs > arms.
5. OPV (Sabin, live, oral) → mucosal IgA + herd immunity but VAPP/VDPV risk; IPV (Salk, killed, IM) → humoral immunity, safe in immunocompromised, no gut immunity.
6. VAPP mostly from Sabin types 2 & 3 (~1 in 2.4 million doses); cVDPV mostly type 2 → reason for tOPV→bOPV switch (April 2016) + IPV; nOPV2 for outbreaks.
7. Diagnosis = isolate virus from two stool samples + RT-PCR intratypic differentiation.
8. Coxsackie A → herpangina (soft palate/uvula vesicles) & HFMD (with A16/EV-71); Coxsackie A24/EV-70 → haemorrhagic conjunctivitis.
9. Coxsackie B → myocarditis/pericarditis (commonest viral myocarditis), Bornholm pleurodynia, pancreatitis/T1DM link.
10. Echovirus/enteroviruses = commonest cause of aseptic meningitis; CSF = lymphocytes, normal glucose, clear; PCR is test of choice.
11. EV-71 = severe HFMD + brainstem encephalitis; EV-D68 = acute flaccid myelitis (polio-like).
12. No routine antiviral (investigational pleconaril, IVIG in agammaglobulinaemia); India polio-free since 2014, last wild case 2011; key complication = post-polio syndrome.