IAS56 Medically Important Viruses

Cell culture is the classic 'gold standard' for viral diagnosis, where a specimen is inoculated onto a cell monolayer, and the virus causes cytopathic effects (CPE) such as plaques (holes where cells die).

The plaque forming unit (PFU) concept estimates infectious virus concentration by counting plaques, which represent infectious particle events.

Key associations include:

• Enterovirus A71: HFMD, can involve CNS
• Coxsackie B: Myocarditis
• Poliovirus: Poliomyelitis (historical)
• Rhinovirus: Common cold (URTI)

Common viral exanthems include:

• HSV
• VZV
• Enterovirus
• Parvovirus B19: 'slapped cheek' rash

Features include:

• Fever
• Sore throat
• Lymphadenopathy
• Atypical lymphocytes
• Rash, especially after antibiotics

High pathogenic coronaviruses include:

• SARS-CoV-1
• MERS
• SARS-CoV-2 (often bat origin with intermediate host)

RT-PCR (Reverse Transcription Polymerase Chain Reaction) is the gold standard diagnostic method for coronaviruses, as it detects viral RNA and is more sensitive than RAT (Rapid Antigen Test).

Clinical features include:

• Cough
• Wheeze
• Feeding difficulty
• Respiratory distress
• Can be severe and life-threatening

Complications of influenza include:

• Pneumonia (often bacterial co-infection)
• Encephalitis
• Myocarditis
• Reye syndrome (children + aspirin)

Key features of dengue fever include:

• Transmitted by mosquitoes
• Symptoms: Fever + rash
• Laboratory findings: ↓ WBC, ↓ platelets
• Severe bleeding with repeat infection

Core CNS viral infections include:

• HSV-1/HSV-2
• Enterovirus
• VZV
• Japanese encephalitis
• West Nile
• Rabies (uniformly fatal)
• Herpes B
• Zika (fetal microcephaly)

Symptoms include cough, wheeze, feeding difficulty, and respiratory distress, which can be severe and life-threatening.

Infant bronchioles are narrow and less supported, leading to inflammation and edema that causes obstruction. This can result in air trapping and hyperinflation with partial obstruction, or collapse (atelectasis) with complete obstruction.

• HA (hemagglutinin): attachment; main neutralizing antibody target.
• NA (neuraminidase): release; target of oseltamivir (Tamiflu).

• Shift: reassortment of segments leading to a new HA/NA combination, potentially causing a pandemic.
• Drift: point mutations over time resulting in seasonal epidemics.

• Upper respiratory tract infection (URTI)
• Pneumonia (often with bacterial coinfection)
• Exacerbation of chronic lung/heart disease
• Encephalitis, myocarditis
• Reye's syndrome (in children on aspirin)

• Elderly
• Young children
• Individuals with chronic diseases
• Pregnant women
• Children on aspirin therapy

• Mosquito exposure
• Symptoms include fever and rash
• Laboratory findings: leukopenia and thrombocytopenia
• Early diagnosis via antigen/PCR; IgM appears later (day 3-5)
• Risk of severe bleeding, especially with repeat infections.

Japanese encephalitis is transmitted through a pig-mosquito cycle, with humans as incidental hosts. It can cause severe encephalitis and is vaccine-preventable. It can also occur via transfusion in immunosuppressed patients.

• HSV-1/2
• Enterovirus
• VZV
• Japanese encephalitis
• West Nile
• Rabies (uniformly fatal if symptomatic)
• Herpes B (from monkey bites/scratches)
• Zika (major fetal risk: microcephaly)

1. History + exam: Identify clinical syndrome.
2. Add exposure risk: Consider travel, contact, sexual history, mosquitoes, transfusion, immunosuppression.
3. Choose the right specimen:
   • Respiratory: NP swab
   • Vesicle: fluid/swab
   • CNS: CSF
   • GI: stool
4. Testing options: Virus-based tests include culture, antigen tests, PCR/RT-PCR, and EM.

• Same virus can cause many syndromes.
• Same syndrome can be caused by many viruses.
• Diagnosis involves combining clinical syndrome, exposure history, correct specimen, and appropriate testing.

The key components of host-based viral diagnosis include IgM/IgG serology and immune response markers.

A significant challenge in viral diagnosis is that many viruses can cause the same syndrome, making it difficult to identify the specific virus responsible. Additionally, one virus can cause multiple syndromes, further complicating diagnosis.

It is foundational because understanding the classification of microbes, virus basics, and clinical syndromes is essential for grasping later microbiology and infectious disease content. The core message is 'Classify or die.'

• Very small; require electron microscopy to visualize.
• Simple structure: genome (DNA or RNA) + protein capsid.
• Some have a lipid envelope, many do not.

1. Attachment to host receptors (viral surface proteins)
2. Entry (often endocytosis)
3. Uncoating
4. Release of genome
5. Transcription/translation of viral proteins
6. Genome replication
7. Assembly
8. Release (may kill host cell)

1. Contact (direct + indirect)
   • Direct: infected person to person (touch)
   • Indirect: fomites (door handles, tables) hand eyes/nose/mouth
2. Droplet
   • Large particles; fall within 1-2 meters
3. Aerosol (airborne)
   • Small particles that float for hours; can travel farther
4. Parenteral
   • Arthropods (mosquitoes/ticks), needlestick, surgical exposure, blood transfusion/transplantation of infected tissues

• Virus kills cells forming plaques.
• A plaque represents an infectious particle.
• Counting plaques helps determine viral load (PFU).

• Affects mouth, palms, and soles.
• Usually mild but can disseminate to CNS or heart.
• Key association: EV-A71 can lead to CNS disease.

Primary presentation: Gingivostomatitis (painful oral vesicles/ulcers, fever).
Reactivation presentation: Cold sores/herpes labialis around mucocutaneous junction (lip/nose).

Primary presentation: Chickenpox (generalized vesicular rash; highly infectious; airborne).
Reactivation presentation: Shingles/herpes zoster (painful dermatomal belt-like vesicles).

Reactivation triggers include:

1. Stress
2. Fever
3. Trauma
4. Hormones
5. Ageing
6. Immunosuppression