Id 6.7

Front 1

Typical Viral Replication Steps

Back 1

Attachment, penetration, uncoating, early protein synthesis, NA replication, late protein synthesis, assembly and release

Front 2

Early viral proteins

Back 2

Generally involved in NA replication

Front 3

Late viral proteins

Back 3

Generally, structural proteins

Front 4

Viral attachment

Back 4

Via specific cell receptor

Front 5

DNA Virus Replication
(generalities)

Back 5

Replicated in host nucleus (except poxvirus)
Use host cell enzymes
Long replication times

Front 6

RNA Virus Replication
(generalities)

Back 6

Replicated in host cytoplasm
(except influenza)
Variable replication time (but may be short)

Front 7

What NA strucutre do you need to translate protein?

Back 7

(+) mRNA
Viral NA comes in multiple flavors. Therefore, imagine the multitude of ways you can create (+) mRNA

Front 8

Viral Release Mechanisms

Back 8

Enveloped viruses: budding (from plasma or nuclear membrane)
Naked viruses: cell lysis

Front 9

Asymptomatic Viral Infection

Back 9

No apparent cellular effect
Potential for transmission to others
Potential long-term complications (i.e. HPV and cervical cancer)

Front 10

Viral Infection Cytopathology

Back 10

May result from a number of different mechanisms (depending on viral life cycle)
May lead to the formation of inclusion bodies

Front 11

Inclusion Bodies

Back 11

Intracytoplasmic or intranuclear accumulations of virions, unassembled virion components or amorphous derbis (think: construction site). Visible under light microscopy and usual in diagnosis (b/c DNA virus, generally leave intranuclear inclusions bodies and RNA viruses leave intracytoplasmic inclusion bodies)

Front 12

Hyperplasia (due to viral infection)

Back 12

Expression of oncogenes, leads to unchecked cell replication. Reason why many viruses are implicated in multiple cancers

Front 13

Viral Infection
(major characteristics)

Back 13

Species, organ, cell specificity
Site of infection: greatest incidence respiratory and gastrointestinal tract (mucosa - not a fortified barrier) but decreased virulence. Skin/CNS infections are less frequent but more symptomatic

Front 14

Viral Infection
(pathogenesis, general)

Back 14

Acquisition, Incubation, Illness, Recovery, Resistance

Front 15

Viral Infecotion
(pathogenesis, acquisition)

Back 15

Airborn, contact, vehicle (i.e. food), vector, placenta

Front 16

Viral Infection
(duration)

Back 16

Persistant vs. non-persistant
Majority of human illness are transient (non-persistant) and relatively short term infections
If persistant, last a lifetime (i.e. HSV)

Front 17

Surface vs. Systemic Non-Persistant Viral Infections

Back 17

Surface: illness occurs at portal of entry (short incubation period)
Systemic: lymphohematogenous spread to distant organ (long incubation period)

Front 18

Interferons
(general)

Back 18

Early, non-specific response to viral infections
Alpha/Beta interferono have the greatest anti-viral effect
(Alpha, the "A" team - produced exclusively by profeossional APCs. Beta, the "B" team - more generalized production by prof/non-prof APCs, i.e. fibroblasts and epithelial cells)

Front 19

Interferons
(mechanism of action)

Back 19

Stimulate host anti-viral protein synthesis (will ultimately block viral protein synthesis)

Front 20

Host Anti-Viral Proteins

Back 20

Methylase
Nuclease
Protein Kinase
Phosphodiesterase

Front 21

Immunopathology (due to viral infections)

Back 21

Type III and IV hypersensitivity (immune complex deposition or attacking infected host cells or auto-immunity against self cells/proteins)