Definition: Virus

Obligatory intracellular parasite with genetic material enclosed in a protein shell

Definition: Capsid

Individual virus particle

Definition: Capsid

Protein coat surrounding nucleic acid

Capsomer

Protein subunites that make up the capsid

Envelope

Lipoprotein coating surrounding the capsid derived from infected cell membrane

Types of Virus symmetry

• Helical
• Icosahedron (platonic solid w/ 12 vertices, 20 faces, 30 edges)

Viral Maturation and Release

• Non-enveloped viruses: cell lysis
• Enveloped viruses: budding

Transforming/oncogenic infection

Infected cells become transformed or oncogenic due to viral effects. Whole viral genome may not be present

Acute/lytic infections

Infected cell is killed rapidly

Latent/proviral infection

Whole viral genome maintained as free or integrated DNA with very limited expression. Can become lytic infection with reactivation

Persistent/chronic/slow

Most cells are not killed and not all cells are infected

Permissive cells

Cells that allow for complete virus replication resulting in virus production

Non-permissive cells

Cells that do not allow for virus growth or virus production

Cytopathic effects (CPE) of viruses

Morphological changes in the host cell

• Cell rounding
• Cell fusion and syncytia
• Inclusion bodies
• Vacuoles

Non-cytocidal viruses

Viruses that do not kill the host cells or produce CPEs (Cytopathic effects). Results in viral persistence, long range effects, and antigenic changes

Cell transformation

Results in loss of contact inhibition and/or aneuploidy (abnormal chromosome numbers)

Inclusion bodies

Aggregates of protein that can be stained

Examples of Inclusion Bodies

1. Pox virus: IB in cytoplasm
2. Herpes virus: nuclear IB, where cell fusion results in many nuclei in a cell
3. RED virus huge irregular inclusion bodies surrounding nucleus
4. Adenovirus: a bunch of intranuclear IB
5. Rabies: cytoplasmic IB (Negri bodies)
6. K9 Distemper: intranuclear + cytoplasmic IB

General Pathogenesis of Viral Infections

1. Entry: usually some sort of receptor attachment
2. Regional lymph node --> primary viremia
3. Spread to organ where it replicates
4. secondary viremia
5. Spread to other target organs of shedding

Orthomyxoviruses

Influenza viruses

• segmented genome
• antigenic variation
• some zoonotic
• hemagglutinin important in pathogenesis

4 Genera of orthomyxoviruses

1. Type A: animal and human
2. Type B: primarily human
3. Type C: Primarily human
4. Thogotovirus

Properties of influenza virus

• Virion morphology: Pleomorphic, enveloped
• Nucleocapsid morphology: helical symmetry
• Negative-sense RNA genome with 8 segments in helical filaments(all essential)
• Nucleic acid replication in nucleus
• Nuclear replication, budding from cell surface
• Hemagglutinin (HA) and Neuraminidase (NA) on surface

Antigenic variation

Antigenic drift: minor changes in HA molecule

• Slow evolution
• Point mutations
• Immunological pressure
• Changes in more than 2 epitopes

Antigenic shift: major Ag change

• Abrupt change that mostly originate in China

Biggest reservoire of Influenza virus in nature

DUCKS get all types of influenza and harbors/excretes virus, but don't get sick!

Molecular basis of virulense and pathogenicity

• HA gets cleaved by host protease into HA1 and HA2 which are linked by disulfide bond.
• Activated HA attach to cell's sialic acid receptors, and endocytosis occurs

Equine Influenza

• H7N7 (Equine 1)
• H3N8 (Equine 2)
• Respiratory, aerosol infection
• Incubation period = 1-3 days
• URI symptoms, fever, secondary bacterial infection
• Recovery 1-2 weeks
• Vaccine: bivalent inactivated vaccine (3 doses 8-12 weeks apart, race horses every 3-6 months)

Avian influenza

• Virulent subtypes - H5, H7
• Hong Kong bird flu - H5N1
• Respiratory signs, edema, diarrhea
• Pantropic spread, high mortality
• Control: quarantine, restrict trade, control wild birds

Swine Flu

H1N1 and H3N2

Human Flu

H1N1

H2N2

H3N2

H5N1

Diagnosis of influenza

Virus isolation

Serology