Picornaviruses & Viral Gastroenteritis
Small RNA viruses of the gut, heart, meninges, and nose
Picornavirus biology
Structure and replication. Picornaviruses ("small RNA") are naked viruses with a positive-sense single-stranded RNA genome. The genome works directly as mRNA, so purified RNA alone is infectious. It lacks a 5′ cap — a small viral protein, VPg, sits at its 5′ end — and ribosomes load at an internal ribosome entry site. Translation yields one long polyprotein that viral proteases cleave into capsid proteins and the RNA-dependent RNA polymerase, which then copies the genome in the cytoplasm. The family includes the enteroviruses, rhinovirus, and hepatitis A (covered in the hepatitis lesson).
| Feature | Enteroviruses | Rhinovirus |
|---|---|---|
| Acid | Stable — survive the stomach | Labile — destroyed in the stomach |
| Spread | Fecal-oral (also respiratory) | Respiratory droplets and hands |
| Season | Summer and fall | Year-round, peaks fall and spring |
| Members | Polio, coxsackie A and B, echovirus, EV-D68, EV-71 | More than 100 serotypes |
Poliovirus
Pathogenesis. Ingested poliovirus replicates in the oropharynx and the Peyer patches of the gut, then spreads by viremia. Most infections stop there; in under 1% the virus invades the CNS and destroys anterior horn motor neurons. The result is asymmetric flaccid paralysis with hyporeflexia or areflexia and fasciculations but intact sensation, legs more than arms. Bulbar polio paralyzes breathing and swallowing. Decades later, survivors may develop post-polio syndrome — new weakness and fatigue in previously affected muscles.
Polio is asymmetric and purely motor; Guillain-Barré syndrome is symmetric, ascending, and sensory as well.
| Feature | IPV (Salk) | OPV (Sabin) |
|---|---|---|
| Type and route | Inactivated, injected | Live attenuated, oral |
| Immunity | Serum IgG blocks spread to the CNS | Serum IgG plus gut IgA that stops intestinal replication and transmission |
| Safety | Cannot cause polio; safe in immunodeficiency | Rarely reverts: vaccine-associated or vaccine-derived paralytic polio |
| Use | Only vaccine used in the US; 4 doses from 2 months | Cheap and oral; global eradication campaigns |
Nonpolio enteroviruses and rhinovirus
- Coxsackie A — herpangina (fever with painful vesicles and ulcers on the soft palate, uvula, and tonsillar pillars) and hand-foot-mouth disease (oral ulcers plus vesicles on palms, soles, and buttocks of young children, classically A16). Enterovirus 71 can add brainstem encephalitis. Both are self-limited summer illnesses.
- Coxsackie B — the classic leading viral cause of myocarditis and pericarditis in young adults (chest pain, arrhythmias, heart failure, possible dilated cardiomyopathy); pleurodynia or Bornholm disease (fever with sudden, stabbing chest-wall or upper abdominal pain from intercostal muscle inflammation); and sepsis-like illness in neonates.
- Echoviruses and other enteroviruses — the most common cause of aseptic meningitis, in summer and fall: fever, headache, neck stiffness, photophobia. CSF shows lymphocytes (neutrophils early), normal glucose, and mildly raised protein; enterovirus PCR confirms, and recovery is complete.
- Enterovirus D68 — wheezy respiratory illness in children and acute flaccid myelitis: sudden asymmetric limb weakness from spinal gray-matter inflammation, a polio-like picture in late-summer and fall outbreaks.
Herpangina ulcers sit at the back of the mouth; HSV gingivostomatitis involves the front — gums, lips, and tongue.
Rhinovirus. Acid-labile and happiest at the cooler 33 °C of the nose, it stays in the upper airway; most strains bind ICAM-1. With more than 100 serotypes and little cross-protection, it is the most common cause of the common cold and a major trigger of asthma exacerbations, and no vaccine exists.
Viral gastroenteritis: rotavirus and norovirus
Rotavirus. A naked, wheel-shaped member of the Reoviridae with 11 segments of double-stranded RNA. It infects mature enterocytes at the tips of small-intestinal villi, blunting the villi and causing watery, nonbloody diarrhea with vomiting and fever. It is the leading cause of severe dehydrating diarrhea in infants and young children worldwide, with winter-spring outbreaks in daycare. Oral rehydration is the mainstay of treatment.
Rotavirus vaccines. Two oral live attenuated vaccines (RotaTeq, 3 doses; Rotarix, 2 doses) start at 2 months; the series must begin by 15 weeks and finish by 8 months of age. They carry a small risk of intussusception (about 1 to 5 per 100,000 infants), mostly in the week after the first dose. Prior intussusception and SCID are contraindications.
Norovirus. A calicivirus (naked, positive-sense ssRNA) and the leading cause of epidemic gastroenteritis in adults and of foodborne outbreaks — cruise ships, nursing homes, schools, and hospitals — peaking in winter. After 12–48 hours, abrupt vomiting (often predominant), watery nonbloody diarrhea, and cramps last 1–3 days. There is no vaccine.
| Feature | Rotavirus | Norovirus |
|---|---|---|
| Genome | Segmented dsRNA (Reoviridae) | Positive-sense ssRNA (Caliciviridae) |
| Typical host | Infants and young children | All ages, especially adults |
| Setting | Daycare; severe dehydration | Cruise ships, nursing homes, restaurants |
| Prevention | Live oral vaccine | Soap and water, bleach, excluding sick food handlers |
Norovirus infects with fewer than 100 particles, spreads by stool, vomit aerosols, food, water, and surfaces where it lasts for days, and resists alcohol sanitizer. Use soap-and-water handwashing and bleach, and keep sick food handlers home until 48 hours after symptoms end — the same soap-and-water rule as for C. difficile spores.