Virus-Host Cell Interactions Flashcards
Non-productive infection
viral infection that doe snot lead to the production of infectious virions
Abortive infection
non-productive infection because the virus lacks virus synthesis post-adsorption
interference non-productive infection
virus interferes with the growth of other viruses in the same cell
Productive infections
successful replication of virus post-adsorption
Productive infections may result in
non-lethal alteration to cell/cell function, cell damage/death, or persistent infection without cell death
Latent-persistent infection
intermittent acute episodes of disease b/w which there is an absence of infectious particles (Herpes simplex)
Chronic-persistent infection
continued presence of virus, disease maybe absent or associated with late immunopathological disease (hepatitis B)
Slow-persistent infection
long incubation, slow progression, lethal disease
Sterilizing immunity
infection is resolved and immunity has been strengthen
Most common outcome of a viral infection is
an asymptomatic infection with a seroconversion
Following an infection damage or death may occur due to
immunopathology or autoimmune induction
Lytic infection
causes cell modification and death; inhibits host macromolecule synthesis, cytopathic effect (toxic to cells), inclusion bodies and cell fusion, apoptosis, chromosomal alterations –>malignancy
Tumor
mass of new tissue which persists and grow independently of its surrounding
Transformation
conversion of cell from restricted growth to unrestricted growth
Transformed cell characteristics
loss of contact inhibition, unrestricted growth, loss of senescence, appearance of new antigens, metabolic and genetic changes
RNA tumor viruses
human T cell leukemia virus (HTLV) target t helper cell
DNA tumor viruses
HPV (cervical cancer), EBV (Burkitt’s lymphoma), HBV (liver cancer)
Benign neoplasm due to viral infections examples
human wart virus, poxvirus
Stages of the virus replication cycle
Attachment, Penetration, Uncoating, Macromolecular Synthesis,
Attachment step of viral replication cycle
virus binds specific receptor (MAJOR determinant of infectivity)
Specific attachment of virus to receptor determines
host range, tissue tropism (where in the body it can survive), target of antiviral therapy
Fusion inhibitors for HIV
target specific HIV receptor on cells and prevent fusion of virion and human cell preventing infection
Penetration step of viral replication cycle (3 ways)
Methods of penetration: Direct penetration, surface eclipse pH dependent, receptor-mediated endocytosis
Direct penetration
NON-enveloped viruses, nucleocapsid attaches to cell surface releasing viral NA genome
Surface eclipse
pH independent cell entry; ENVELOPED viruses fuse with the CM releasing viral NA
Receptor-mediated endocytosis
ENVELOPED virus binds specific receptor, endocytosis occurs, virus envelope fuses with endosome membrane to release viral genome
Uncoating step of viral replication cycle
removal of protective coats with release of NA; infectivity is lost at this point
What two antivirals inhibit the uncoating step of Influenza A.
Rimantidine and Amantidine
Macromolecular Synthesis step of viral replication cycle
synthesis of viral encoded proteins and viral genome
DNA viruses replicate in the
nucleus
RNA viruses replicate in the
cytoplasm
Pox virus (DNA) replicates in the
cytoplasm
Influenze virus (RNA) replicates in the
nucleus
(+)ssRNA, (-)ssRNA, dsRNA all
encode for RNA-dependent RNA polymerase
The exception to all RNA viruses needing to encode for RNApol is:
retroviruses (HIV) they encode for reverse transcriptase which transcribes DNA from RNA, then to mRNA
azidothymidine AZT, ddI, ddC, 3TC, D4T
nucleoside analogue reverse transcriptase inhibitor (NRTI) - target for HIV
(-)ssRNA and dsRNA must carry
gene for RNApol and RNApol protein to transcribe the mRNA
(+)ssRNA must carry
ONLY the gene for RNApol
RNApol is capable of
transcribing the mirror image of the strand (complimentary strand)
DNA viruses replicate
using host cell DNA replication machinery
RNA viruses replicate
using encoded RNApol, and some require RNA pol proteins
The exception is HIV retrovirus which replicates
using reverse transcriptase (ssRNA –> dsDNA (inserted into genome)–>mRNA)
Integrase inhibitor
prevents the insertion of HIV DNA into the genome for replication
Cidofovir
inhibitor of nucleic acid synthesis - nucleotide analog (smallpox treatment)
Acyclovir, Valacyclovir, Famciclovir, Penciclovir, Ganciclovir
inhibitor of nucleic acid synthesis - nucleotide analog (human herpes viruses 1-8)
Foscarnet
inhibitor of nucleic acid synthesis - nucleotide analog (CMV and HSV)
Viruses may be released from cells in 3 ways
lysis of cells, slow release without lysis, or budding
Budding
Viral proteins cluster and replace all host proteins in that segment of the CM, nucleocapsid bind to viral proteins and an enveloped virus is released
Neuraminidase inhibitors (oseltamivir, sanamivir)
selectively inhibit neuraminidase of Influenza A and B
HIV protease inhibitors prevents the viral protease that initially cleaves the proteins to functional proteins , these are:
Saquinavir, indinavir, amprenavir, nelfinavir, ritonavir
Primary replication site
site where 1st replication takes place, if near port of entry = short incubation period
Secondary replication site
site where 2nd replication takes place
Local spread ___________ occurs, spread within host _________ occurs
always ; may
Spread within a host may occur through
cell-to-cell, bloodstream, lymphatics, nerves, transplacentally
