Viruses cont'd

Question 1

Which type of influenza virus is most common?

Answer 1

type A - associated with most concerns

Question 2

Influenza types genome segments

Answer 2

A =8
B =8
C=7

Question 3

Influenza replication

Answer 3

attachment brings cell and virus membranes into proximity -> conformation change triggered after cell attachment by pH change in endoscope -> causes membrane fusion -> transcription and replication in nucleus -> protected genome (RNP core) escapes nucleus and buds from cell surface - NA critical to budding

Question 4

When virus replication is a model to all enveloped viruses?

Answer 4

influenza

Question 5

influenza prevention and control

Answer 5

attenuated live vaccine
- antigenic shift (virus mutations) require new vaccine every year
antiviral treatment
- amantidine, rimantidine
- block entry, inhibits M2 activity
- development of resistance common
- Zanamivir or oseltamivir (tamiflu) - blocks release of budding visions, development of resistance not common

Question 6

Influenza pandemics

Answer 6

Pandemics thought to arise from avian strains
1918 spanish flu = H1N1 strain; virulent in healthy adults, cause “cytokine storm” in lethal cases
1957 Asian flu = H2N2 strain; deaths mostly in elderly and young children
1968 Hong Kong flu = H3N2
2009-2010 H1N1

Question 7

3 phases of gene expression in adenovirus

Answer 7

immediate-early: E1A portion of genome
- 2 transcriptional regulators (cell and virus)
- necessary to reach early stage
early: 5 genome sections
- E1B, E2,E3,E4,L1
- DNA replication and post transcriptional events
late
- take over cellular mRNA synthesis

Question 8

Adenovirus replication

Answer 8

initiated on either end, identical end sequences -> replication in 5’ to 3’ direction, one strand displaced -> displaced strand circularizes to allow template copy to be made -> primed by protein pTP, unusual priming strategy

Question 9

Alphaherpesvirus latency period

Answer 9

stationary cells, genome circularizes and stays as an episome in nucleus
- peripheral ganglia common site of latent infections

Question 10

Triggers of alphaherpesvirus

Answer 10

sunburn, systemic infection, immune impairment, stress

Question 11

Alphaherpesvirus control

Answer 11

cell mediated immune response required

• people unable to produce Ab can still handle herpesvirus infections
• T lymphocytes detect antigens presented by MHC I or II proteins

Question 12

How does herpesvirus counteract immune response?

Answer 12

viral proteins bind Ab and complement proteins

- counters effects of interferon

Question 13

Alphaheresvirus prevention and treatment

Answer 13

prevention: avoid contact during active herpes recurrence
treatment: acyclovir can be used to limit virus replication
- will not eliminate latent infections

Question 14

How does beta/gammaherpesvirus evade immune system?

Answer 14

intrinsic = block cell death, inhibit apoptosis
innate = decrease NK cell activity, inhibit NK receptor activation
adaptive = decreased antigen presentation, degrade MHC I and II, block MHC II and T-cell receptor interactions

Question 15

CMV persistence and latency

Answer 15

• persist hematopoietic progenitor cells and macrophages in vitro
• chronic persistent infection, not latency
• controlled by healthy, active immune system

Question 16

EBV persistence and latency

Answer 16

• persistence of genome in memory B cells

- virus proteins ensure B cell proliferation and EBV genome replication

Question 17

Beta/gamma antiviral therapy

Answer 17

• recommended for disseminated CMV and EBV in immune compromised individuals
• ganvivlovir, foscarnet, acyclovir - inhibit viral genome replication, resistance can develop during therapy, less effective treating EBV induced (genome replication not essential for viral gene expression)
• pyophylactic or preemptive treatment, common in transplant patients

Question 18

Beta/gamma immunoprophylaxis

Answer 18

• passive transfer of Ab for prevention of CMV infection

- transfer of EBV-specific T lymphocytes