Viruses Flashcards
Nucelocapsid
Genetic material and structural proteins
3 types of capsid symmetry
Helical/tubular
Icosahedral
Complex
Properties of naked vs enveloped virsuses
Naked: environmentally stable, spread easily, can survive gut/drying/detergents
Enveloped: environmentally labile, must stay wet, cannot survive GI tract
How do naked vs enveloped viruses leave a cell?
Naked: cell lysis
Enveloped: budding and cell lysis
7 general steps of viral replication
Adsorption (attachment) Entry Uncoating Transcription Synthesis of virus components Assembly Release
Tropism
The interaction between specific proteins on a viral surface and specific receptors on a target cell membrane
2 mechanisms of viral entry
Endocytosis
Fusion of virus envelope with cell membrane
Synthesis of new DNA viruses
Replication of DNA in host cell nucleus mediated by viral enzymes
Capsid and other proteins synthesized in cytoplasm using host cell enzymes
How are + sense RNA transcribed differently from - sense RNA
+: acts as mRNA, viral proteins are made immediately in cytoplasm by viral enzymes
-: first makes a + sense RNA copy via viral enzymes
Reverse transcriptase
HIV
Converts + sense viral RNA to cDNA, which is then integrated into host cell chromosome
Host cell enzymes make the mRNA from viral DNA
3 types of persistent viral infections and an example of each
- Chronic carrier (Hep B)
- Latent infection (herpesviridae)
- Slow virus infections (Measles virus-Rubeola, due to prolonged incubation period)
Horizontal transmission examples
Direct contact Respiratory Fomites Insect vector Zoonoses
Potential sites of action for antiviral agents
Attachment to the host cell Uncoating of the viral genome Genome replication Assembly of progeny virions Release of virus particles from the host cell
How does HIV enter the cell?
Binds to CD4
Rolls and binds to co-receptor (CCR5 or CXCR4)
Virus cell fusion occurs
2 general ways to prevent viral attachment
Agents that mimic the virus attachment protein and bind to cellular receptors
Agents that mimic the receptor and bind to the viral proteins
Maraviroc (Celsentry)
Selective for CCR5
Blocks the CCR5-gp120 interaction (binds to CCR5)
Prevents CCR5 tropic HIV entry into cells
Enfuvirtide (Fuzeon)
Mimics amino acids of HIV gp41 that are critical for viral/CD4 cell membrane fusion
Prevents viral entry
Attaches to gp41 and prevents the interaction
Nucleoside reverse transcriptase inhibitors
Competitive inhibitors of reverse transcriptase
Compete with natural nucleosides
Inhibit chain elongation (lack the OH needed for bonding)
Why would you take multiple reverse transcriptase inhibitors at once?
So multiple base analogs are present and you can block the inhibition in many places
Non-nucleoside reverse transcriptase inhibitors
Prevent HIV from using reverse transcriptase by binding at an allosteric site
Why would you use multiple drugs to treat HIV?
Resistance is rapidly encountered during monotherapy (ex: mutation in the reverse transcriptase)
Can block the proliferation at many different spots
Using more drugs with more targets reduces the emergence of resistant mutants
Protease inhibitors
Protease inhibitors prevent post-translational cleavage of Gag-Pol polyprotein
Results in immature, noninfectious viral particles
Prevents other cells from being infected
Integrase inhibitors
Ex: Raltegravir
Binds viral integrase, inhibits strand transfer
Interferes with integration of reverse-transcribed HIV DNA (cDNA) into the chromosome of host cells
HAART
Highly active anti-retroviral therapy
Acyclovir
Used to treat herpes
Competition with deoxyGTP for the viral DNA polymerase resulting in:
1. it binding to the DNA template as an irreversible complex
2. chain termination following incorporation into the viral DNA
What do the H and N stand for in flu strains?
H: hemagglutinin
N: Neuraminidase
Amantadine
For influenza
Blocks the M2 proton ion channel of the virus and inhibits uncoating of the viral mRNA
Tamiflu (oseltamivir)
For influenza
Analog of sialic acid (decoy basically)
Interferes with the release of progeny influenza virus from infected to new host cells
Halts the spread of infection
Competitively and reversibly interacts with the active enzyme site to inhibit neuraminidase activity and destroy the receptors recognized by viruses