L49: Medically Important Viruses Flashcards
Picornavirus (big family)
- Enterovirus:
- Rhinovirus (Respiratory route, URT infection)
- Enterovirus (GI/faecal-oral route, systemic infection e.g. poliovirus) - Paraechovirus
- Hepatovirus
Pathogenesis of Enterovirus
- no lipid envelope
- Stability in environment: can survive external environment, gastric acidity and faecal enzyme
- Asymptomatic infection (Iceberg effect): multiply in intestinal lymphoid tissue, remain undetected and can still transmit from asymptomatic persons
- Flu-like illness: viraemia —> fever
- Full disease syndrome: organ dysfunction: poliomyelitis, meningitis, encephalitis, myocarditis
- DO NOT cause diarrhoea
- Once recover immunity is lifelong, no mechanisms for persistence
Enterovirus 71
Hand,foot and mouth disease
Polio vaccine
Type 1, 2, 3 (type 2 + 3 now eradicated)
Multivalent (Type 1, 2, 3)
- Oral live attenuated (one live virus each time, at least 3 doses)
- easy to administer, mucosal immunity —> block transmission
- virulence reversion
- now type 2 oral vaccine removed —> IPV only - Killed (3 dose: primary, secondary and booster)
Pathogenesis of Herpesviridae
- double stranded DNA virus
- Enveloped
- Virus latency (within any level of spinal cord): Once infected —> always infected
- Viral genome: integrated / episomal
- Genome not completely expressed
- Viral antigens not visible on cell surface: evade host immune mechanism
- Trigger from latency to full replication (from time to time): Lysogenic cycle —> Lytic cycle —> can spread to others
Herpes simplex type 1 vs Herpes simplex type 2
HSV1 (above waist)
- Often asymptomatic
- Mild oral lesions to severe stomatitis
- Herpetic whitlow
- macule vs papule
- vesicle vs pustule
- ulcer
HSV2 (below waist)
- genital herpes
Primary infection and recurrence of HSV and VZV
Primary
HSV: mild pharyngitis, fever, genital herpes
VZV: chickenpox
Recurrence (depends on latency in which level of spinal cord)
HSV: cold sore, genital herpes
VZV: shingles / herpes zoster
Pathogenesis of Influenza virus
- Type A, B, C
- RNA virus (single stranded, negative sense)
- segmented genome
- Haemagglutinin H1-H16: bind to sialic acid on host cells
- Neuraminidase N1-N9: cleaves Terminal sialic acid —> virus release
- Antigenic drift and Antigenic shift
Antiviral drugs (4 classes)
- Amantadine/ Rimantadine: Block virus uncoating
- Oseltamivir, Zanamivir: Neuraminidase inhibitor
- Baloxavir marboxil: cap-dependent endonuclease inhibitor (interfere with replication process)
(4. Favipiravir: polymerase inhibitor)
Symptoms of flu
Often caused by cytokines by host immune system (not the virus going to different body parts)
Host immunity
- Cell-mediated response: helps recovery
- Humoral response: Antibody bind to Neuraminidase and Haemaglutinin —> neutralises infectivity
Antigenic Drift vs Antigenic Shift
Drift: Minor antigenic change from MUTATION since RNA polymerase lack proof reading mechanism
Shift: Complete change of H and N antigen due to GENETIC REASSORTMENT: mixing of 2 viral genes (human and animals)
Prevention of influenza
- Vaccine: need to identify new antigenic drift variants
- Antiviral: Oseltamivir / Zanamivir (Amantadine / Rimantadine not used anymore)
- Hygiene