68 terms

Viruses on Host Pages 41 - 52

Cytocidal, Non-cytocidal, Cell Transformation
3 Classifications of Viral Effects on Host Cells
Nonproductive infections
Cell changes leading to cell death or transformation may occur in
Persistant Infection
Slow release of virus without cell death
Latent Infection
Virus present but not causing harm to cell; later emerges in lytic infection
Lytic Infection
Death of cell and release of virus
Cytopathic Effect (CPE; Cell Injury)
Defined as visible or morphologic changes induced in a host cell by a virus that may result in host cell damage and/or death.
Cytopathic Effect
Secondary effects of virus' metabolic needs and not simply toxic effects of viral proteins on host cell
Cell Lysis, Cell Rounding and Detachment, Inclusion Bodies, Syncytium Formation, Cytoplasmic Vacuolation, Cell Transformation, and Cell Membrane Changes
7 Cytopathic Effects on host cells
Inclusion Bodies
Morphologic change in cells infected by some viruses, intracellular structures (H&E stain); Aid in identification of viruses
Cytocidal Viral Infections
Inhibition of host cell DNA replication, Selective inhibition of cellular mRNA production, Inhibition of Cellular mRNA export. These are mechanisms of what?
Cytocidal Viral Infections
Shutdown of host cell protein synthesis while viral protein synthesis continues, Some viral proteins cause the cell's lysosomes to release their enzymes resulting in destruction of intracellular contents and host cell death. These are mechanisms of what?
Cytocidal Viral Infections
(Effects on membrane) Promotion of cell fusion (syncytia); Altering membrane permeability. These are mechanisms of what?
In general, _________ are prone to premature cell death.
Cell Fusion
This may promote cell-to-cell spread of viruses (type II). Also a side product of virus penetration.
Cytocidal Viral Infections
Changes in cell shape caused by damage to the cytoskeleton; Apoptosis; Cytolysis by immunologic Mechanisms (ADCC). These are mechanisms of what?
Microfilaments, Intermediate Filaments, Microtubules
These 3 things make up the cellular cytoskeleton and maintain the structural integrity of cells and help in transport of organelles.
These viruses infect cells and actively produce infectious viral particles WITHOUT causing immediate death to host cells. Often persistent infections
Cell Transformation
The changing of normal cell into a cancer cell.
Cell Transformation
Multistep process involving mutation and selection for cells with progressively increasing capacity for proliferation, survival, invasion, and metastasis.
Proliferation, Survival, Invasion, Metastasis
Cells for the development of cancer are selected based on their capacity for these 4 things.
Cell Growth, Division, Differentiation
Proto-oncogenes are genes whose protein products function in the signal transduction pathways that control these 3 NORMAL processes.
Not of viral origin, viruses may contain a form of these that went through genetic recombination
1) Secreted growth factor proteins 2) Transmembrane growth factor receptors 3) Intracellular signal transducers 4) Proteins that affect cell proliferation by activating nuclear transcription; Are all products of what?
A proto-oncogene can be converted into this by point mutation, deletion, DNA rearrangement, or insertion of mobile genetic element such as retroviral DNA.
Genes whose products can transform normal cells. They are abnormally expressed or mutated forms of another cell induced by carcinogens or viruses.
Products of oncogenes that are unregulated. May cause uncontrolled proliferation or inhibit apoptosis.
Tumor Suppressor Genes
Genes that encode proteins that normally inhibit cell proliferation.
G1 Phase
Tumor Suppressor Genes hold the cell cycle at this phase
Rb Protein
Inhibits the entry of cells into S phase.
Retinoblastoma protein and p53 protein
2 Negative regulators of proliferation
Rb gene
Normally expressed in almost all cells of the body.
Rb protein
Alternates between a phosphorylated state (promoting DNA replication) and an unphosphorylated state (inhibits DNA synthesis)
p53 protein
In addition to mediating cell cycle arrest, this protein is required for apoptosis induced by DNA damage.
Cells lacking p53 cannot undergo this process in response to damage of DNA.
T/F All known oncogenic viruses either have a DNA genome or generate a DNA provirus after infection.
The only RNA viruses that are oncogenic are in the family reoviridae.
Permissive Cell
DNA tumor viruses interact with cells two ways, one is: Productive infection, in which the virus completes its replication cycle, resulting in cell lysis. Name the cell type.
Nonpermissive Cell
DNA tumor viruses interact with cells two ways, one is: Nonproductive infection, in which the virus transforms the cell without completing its replication cycle. Name the cell type.
Polyoma-, Adeno-, Herpes-, Hepadna-, Papilloma-, Poxviridae
5 DNA Families that can be oncogenic
DNA oncogenes
_______ have no counterpart in the normal host cell.
DNA oncogenic viruses activate the host cell's replication machinery by _______ the action of key tumor suppressor genes.
DNA oncoproteins bind to Rb and p53 proteins _________ them.
T/F A characteristic property of RNA tumor viruses is that they are not lethal for the cells in which they replicate in, hence virus infection is both productive and oncogenic.
Acute Transforming Viruses [v-onc+]
They possess v-onc genes. that are derived from host cell proto-oncogenes.
T/F Oncoproteins coded by v-onc genes have no role in virus replication.
Chronic Transforming Retroviruses [v-onc-]
The viruses lack v-onc genes and are weakly oncogenic.
Altered Cell Morphology, Chromosomal Abnormalities, Capacity to Divide Indefinitely (due to contact inhibition), Virus Specific Tumor Associated Antigens, Produce Malignant Neoplasms
5 Characteristics of Transformed Cells
This is a heritable change in the nucleotide sequence of the genome of an organism. It is the MOST FREQUENT cause of genetic change in viruses.
Lethal, Neutral, Selective Advantage
Mutations can be (3 things)......
T/F The error rate in viral DNA is greater that that of RNA.
Escape Mutants
Mutations affecting antigenic determinants of virion surface proteins, affect sensitivity of progeny to neutralizing antibody. Persistent Infections
Conditional-lethal mutants
Results from mutations that so affect a virus that it cannot grow under certain conditions [nonpermissive conditions], but can repli cate under other, permissive, conditions.
Temperature-sensitive [Ts] mutants
Grow at low [permissive] temperature but not at high [nonpermissive] temperature. Been used in attempts to produce attenuated live-virus vaccines
Defective interfering [DI] mutants
A virus that lacks one or more functional genes required for viral replication due to a deletion mutation. They require infectious homologous virus as helper for replication; in the process, they interfere with and usually decrease the yield of the helpervirus.
T/F DI Particles may play a role in persistent infections by attenuating the lethality of the parental infectious virus.
Dual Infection
Interactions among viruses. If the viruses are dissimilar, they may replicate within the same cell as efficiently as in single infections. This is know as...
Genetic Interactions
Interactions among viruses. These are interactions involving the genomes of the parental virions. Resulting progeny are genetically different from either parent.
Genetic Recombination
This involves breaking of the nucleic acid strands, and part of the genome of one parent is joined to part of the genome of the second parent. New virus is genetically stable.
False, some exceptions
T/F All viruses with genomes that consist of ssRNA do not recombine.
Genetic Reassortment
This is the exchange of complete RNA molecules between genetically related viruses with segmented genomes.
Nongenetic Interactions
Interactions among viruses where the products of the genes that interact rather than the genomes. Thus, progeny produced are similar to the parents.
Phenotypic masking or mixing
When two closely related viruses infect the same cell, the two types of progeny genomes may become encapsidated not only by their own capsids but also by hybrid capsids.
The extreme form of phenotypic mixing.
T/F Phenotypic mixing or masking can occur among enveloped viruses involving both related and unrelated viruses.
Viral Interference
Occurs when the multiplication of a superinfecting virus in cell culture or in the host is inhibited because of the presence of an initially infecting virus.
Viral Pathogenesis
This is concerned with the method by which viruses produce disease, ie, the mechanisms by which viruses injure discrete populations of cells in different organs and tissues to produce the signs and symptoms of disease in a particular host.
T/F Majority of viral infections are subclinicaI and do not result in disease.
T/F The same disease may be produced by different viruses. The same virus may produce a variety of diseases