Block 3 Flashcards
Cytopathic effect (CPE)
Damage or morphological changes to host cells during virus invasion
Cell fusion (Syncytium or polykaryon formation)
Fusion of the plasma membranes of four or more cells to produce an enlarged cell with four or more nuclei. Prone to premature cell death.
Inclusion bodies
An abnormal structure in a cell nucleus or cytoplasm or both, such as aggregates of proteins, having characteristic staining properties and associated with certain viral infections. Helps to identify certain viral infections.
Inclusion bodies can be: (3)
1) accumulation of viral components
2) result from degenerative changes in cell
3) crystalline aggregates of virions
Intrinsic (Mitochondrial) Apoptotic Pathway
Activated as a result of increased permeability of mitochondrial membranes subsequent to cell injury, such as that associated with a viral infection
Extrinsic (Death Receptor) Apoptotic Pathway
Activated by engagement of specific cell-membrane receptors, which are members of the TNF receptor family (TNF, Fas, and others). Thus binding of the cytokine TNF to its cellular receptor can trigger apoptosis.
Cell transformation
The changing of a normal cell into a cancer cell
Neoplasia
Abnormal tissue overgrowth that may be either localized or disseminated. Process that leads to the formation of neoplasms.
Oncology
The study of neoplasia and neoplasms
Benign neoplasm
Growth produced by abnormal cell proliferation that remains localized and does not invade adjacent tissue
Malignant neoplasm (syn. cancer)
Locally invasive and may also be spread to other parts of the body (metastasis)
Oncogenic viruses
Viruses that cause or give rise to tumors
Metastasis
Spread of cancer cells from the part of the body where it started (the primary site) to other parts of the body.
Proto-oncogenes
Encode proteins that function in normal cellular growth and differentiation
Tumor supressor genes (and examples)
Plays a role in keeping cell division in check. Encodes proteins that regulates and inhibits uncontrolled growth.
Rb and p53
Oncogenes
Mutated forms of proto-onco genes or aberrantly expressed proto-oncogenes
Retinoblastoma Protein (Rb)
One important tumor supressor gene/protein that blocks E2F and keeps cell division in check. E2F facilitates cell division.
p53
Tumor supressor gene/protein that prevents cells with damaged DNA from entering into cell division. Tries to mediate repairing of the damaged host cell DNA. If the damaged DNA cannot be repaired, p53 mediates apoptosis of the cell with damaged DNA.
Tumor Virus/Oncogenic Virus
Virus that causes cancer
Oncogenic viruses generally have a ____ genome, or generate a ____ after infection (Retrovirus)
DNA genome; DNA provirus
Oncogenic DNA viruses
Have the viral oncogene in the viral DNA. These oncogenes cause cancer in host cell, and also may help in the virus replication process.
Productive infection of Oncogeneic DNA Viruses in Permissive Cell
Virus complete its replication cycle, resulting in cell lysis = NO CANCER
Non-Productive infection of Oncogeneic DNA Viruses in Non-Permissive Cell
Virus transforms the cell without completing its replication cycle = CANCER
Oncogenic RNA Viruses –> Acutely Transforming Retroviruses
These viruses steal the proto-oncogene from the infected host cell DNA, and then the virus converts the proto-onogene into the oncogene (v-onc, cancer causing gene)
Oncogenic RNA Viruses –> Slow/Chronic Transforming Retroviruses
Virus genome gets inserted into the regulatory (enhancer region) gene of host cell DNA. As a result of this insertion, the regulatory gene cannot function properly. There is no control on proto-oncogene of host DNA. The result is excessive cell division, or cancer.
Tumor antigen
New antigens appear on the surface of tumor cells that may provoke an immune response
Feline oncornavirus membrane-associated antigen (FOCMA)
Example of expression of tumor antigens
Pathogenicity
Ability of a virus to causes disease in host (ie harm the host)
Pathogenesis
Manner/mechanism of development of a disease
Virulence
Quantitative or relative measure of the degree of pathogenicity of the infecting virus
Avirulent
Not virulent (not harmful to the host)
Lethal dose 50 (LD50)
Dose of the virus required to cause death in 50% of animals
Infectious dose 50 (ID50)
Dose of virus that will infect 50% of an experimental group of hosts/animals
T/F: The lower ID50 and LD50, the more virulent the organism
TRUE
Disseminated Infection
Infection spreads beyond the primary site of infection
Systemic Infection
If a number of organs or tissues are infected
Apical vs Basolateral release of virus
Apical: facilitates virus dispersal
Basolateral: Provides access to underlying tissues, facilitates systemic spread
Viremia
The presence of a virus in the blood. Virus may be free in blood or in a cell, such as lymphocytes.
Primary Viremia
Initial entry of virus into the blood after infection
Secondary Viremia:
Virus has replicated in major organs and once more entered the circulation
Passive Viremia
Direct inoculation of virus in blood. No initial replication elsewhere in host before. Ex: bite of arthropods or contaminated syringe
Active Viremia
Viremia following initial virus replication in host. Release of virions from the initial site of replication, such as lymphatics or epithelium of intestine, to the blood stream.
Neurotropic Virus
Viruses that can infect neural cells/ Infection may occur by neural or hematogenous spread.
Neuroinvasive Virus
Viruses that enter the CNS (spinal cord and brain) after infection of a peripheral site
Neurovirulent Virus
Viruses that cause disease of nervous tissue, manifested by neurological symptoms and often death
Herpes Simplex Virus
Low neuroinvasiveness; High neurovirulence.
It always enters the peripheral nervous system, but rarely enters the central nervous system. When it does, consequences are almost always severe, if not fatal.
Mumps Virus
Exhibits neuroinvasiveness, but low neurovirulence. Most infections lead to invasion of CNS, but neurological disease is mild.
Rabies Virus
High neuroinvasiveness and high neurovirulence. It readily infects the peripheral nervous system and spreads to the CNS with 100% lethality unless antiviral therapy is administered shortly after infection.
Retrograde Spread
Travel opposite direction of nerve impulse flow. Invades axons then spreads to dendrites.
Anterograde Spread
Travel in direction of nerve impulse flow. Invades dendrites then spreads to axons.
Localized Acute vs Systemic Acute Infections: Site of pathology
Localized: Portal of entry
Systemic: Distant sites
Localized Acute vs Systemic Acute Infections: Incubation Period
Localized: Relatively short
Systemic: Relatively long
Localized Acute vs Systemic Acute Infections: Viremia
Localized: no
Systemic: yes
Localized Acute vs Systemic Acute Infections: Duration of immunity
Localized: variable, may be short
Systemic: mostly life long
Localized Acute vs Systemic Acute Infections: Secretory IgA
Localized: Very important
Systemic: Not important
Acute Infection
Usually intensive shedding over short time periods
Persistent Infection
Can be shed at lower titers for months to years
Tropism
The specificity/affinity of a virus for a particular host tissue
Pantropic Virus
Can replicate in more than one host organ/tissue
Virus Injury to skin: Vesicles
Fluid filled sacs/elevations
Virus Injury to skin: Ulcer
Opening in the skin caused by sloughing or necrotic tissue, extending past the epidermis
Virus Injury to skin: Nodule, tumor
Palpable, solid, elevated mass. Nodules with distinct borders. Tumors extending deep into the dermis.
Virus Injury to skin: Warts
Benign skin growths that appear when a virus infects the top layer of the skin
Virus Injury to skin: Papule
Solid elevations without fluid with sharp borders
Virus Injury to skin: Erythema
Reddening of skin, consequence of systemic viral infections (endothelial injury in blood vessels throughout the body, including those of the subcutaneous tissue)
Teratogenesis
The abnormal DEVELOPMENT or arrests in development of embryo or fetus. May result in death or malformations during the antenatal period.
Infectious Bursal Disease
Example of virus-induced immunopathology. Virus replication causes atrophy of the bursa and a severe deficiency of B lymphocytes, resulting in immunosupression. As a result, infected birds become susceptible to other pathogens.
Inapparent Infections (4)
- Clinical signs and symptoms are not evident
- Too few cells may be infected
- Stimulate host immune response
- Possible source of virus spread
Acute/Short-Term Infection
Short clinical course. Rapid clearance from host immune response.
Latent/Persistent Infection
Infectious virus is not demonstrable except when reactivation occurs. Reactivation is often stimulated by immunosuppression and/or by the action of a cytokine or hormone. Ex: cold sores
Chronic/Persistent Infection
Acute infection followed by chronic infection in which the virus is continuously shed from or is present in infected tissue
Slow/Persistent Infection
Prolonged incubation period, lasting months or years. Slow progressive lethal disease.
How does Canine Distemper Virus cause CNS damage?
Progressive Demyelination
How does Prion Disease cause CNS damage?
Neuronal Vacuolation
Petechiae Hemorrhage vs Ecchymoses Hemorrhage
Petechiae=pin-point/small spots
Ecchymoses=larger areas, ill-defined margins
Disseminated Intravascular Coagulation (DIC)
Clots form in small blood vessels throughout the body which causes organ failure. In later stages, material for clot is exhausted due to over use, so there is no longer clot formation in later stages, which causes hemorrhages throughout the body.
Virus-induced immunopathology
Tissue injury mediated by host immune response to virus infection. It is the price paid by the host to clear a viral infection.
Routes of viral entry to the skin (3)
1) Transcutaneous Injection (bite of arthropod)
2) Bite of infected animal
3) Contaminated objects
Defense mechanisms of the skin (6)
1) Dense keratin
2) Low pH
3) Fatty Acids (sweat)
4) Bacterial flora
5) Dryness
6) Innate & Adaptive Immunity
Routes of viral entry (4)
1) Skin
2) Mucus Membrane
3) GI Tract
4) Respiratory Tract
Arthrogryposis
Joint constrictures of fetus
Fetal pathogenesis from BVDV (2)
1) Porencephaly
2) Congenital hydranencephaly (slight dome-shaped skull)
