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19 Cards in this Set

  • Front
  • Back
viral pathogenesis is determined by what?
entry route, mechanism of spread bw hosts, spread within host, tissue tropism, direct effects of infection upon cells, interaction with immune system, host variability, and combinations of these factors to determine the out come of the infection
what viruses enter through respiratory epi?
rhino, orthomyxo, paramyxo, adeno, and corona
what viruses enter through the alimentary tract?
rota, picorna, calici, astro (calici and astro cause Hep A)
what viruses enter through the skin epi?
herpes, pox, paplloma, arbo
what viruses enter through the conjunctiva?
rhino, enter 72, adeno, HSV
what viruses enter through the sexual mucosae?
HSV, HIV, hep B
what viruses enter congenitally (blood)?
HIV, CMV, rubella, HSV
what viruses enter perinatally? (during birth)
describe the different types of transmission?
human to human (horizontal): resp, fecal oral, sex, close contact, ~arthropod borne. Human to human (vertical): congenital, perinatal, breast milk, retroviral germ line transmssion seen in mice but not humans. Animal to humans (zoonoses): bite, scratch, contact, consumption, inhalation of excretia, urine in cut, most arthropod borne
where can viruses shed?
resp/oropharyngeal secretions, feces, skin (not all viruses that cause a rash can be spread by skin), urine (CMV and mumps), milk (HTLV and HIV), genital secretions, blood
factors that determine if a virus can infect a given vell within a host tissue
accessibility of the permisive cell (depends on route of spread and physical barriers), presence of appropriate cell surface receptors, presence of intracellular host factor required for virus replication, absence of suppressive antiviral mediators (most important is interferon)
once infected describe the various routes the virus can spread through the body.
local spread: influenza from URT to lung epi, norwalk in GI only. Infected cell-associated: replicate in mac or lymphocyte and spread inside the cell, HIV hits the T cells, T cells circulate to spread, arboviruse infect dendritic cells in the eskin which then migrate to the draining lymph node. viremia: most effective, rapid, and common, arbovirus, measles, VZV; polio itself will go GI, viremia, CNS; can be cell associated before viremic. nerve travel like herpes from skin to CNS and ganglia then back to skin or rabies via axon xytoplasm, few viruses like arb travel from olfactory epithelium to axon. transplacental spread from viremia or cell associated, rubella, HIV1, CMV. transovarily: some arbo viruses infect the egg then offspring, some retroviruses are integrated in germ line (mice only)
how can viruses get to the CNS?
hematogenous is the most common means, usually early host response to infection (cytokines) increases permeability to CNS. Infecting BV's of meninges (mumps) or choroid plexus with invasion of neurons via the CSF. Direct travel via peripheral nerve as in rabies, VZV, and herpes. in infected phagocytic cells like macs and dendritic cells (HCMV and arbovirus). CNS infection maybe after acute disease due to infection in the periphery.
what are the outcomes of infection at the single cell level?
cell death is most common with production of daughter viruses (apop or necro). Abortive infection possibly due to lack of favorable conditions, cell can be damaged , transformed or killed in some cases but no progeny virus is made. Initial hyperplasia followed by necrosis. persistent infection - cells are not altered significantly in their growth habits other than rate, can be chronic, latent, recurrent, or transforming
describe the innate antiviral immunity and what it is comprised of.
low speceficity and forms mainly barriers. Composed of barriers to entry like keratinized epi and mucous layers, phagocytes like macs, dendritic cells, neutrophils and the cytolytic NK cells; anti pathogen and inflammatory cytokines including interferon, TNF, IL1, 12, and 6; and complement
describe the antiviral adaptive immune response.
important players are CD8 and Ab producing B cells, but CD4 is invovled. Ab primary activity is recognizing glycoproteins on the viral envelope and capsid proteins on non enveloped and then neutralizing their infectious ability. Ab can also bind to proteins expressed on the virally infected cell and decrease viral replication within that cell. CD8 cells recognize and kill virus infected cell... this can be a problem when they kill infected cells that do not regenerate like neurons
describe the immunopathology associated with viral disease.
flulike symptoms from cytokines and other mediators is the most common. Over stimmulation of innate immunity via pro inflammatory cytokines can result in immune suppression and schock. Viral pneumonia can be from over stimulation of innate and adaptive immunitiy after viral damage to LRT ciliated epi, common in children with parainfluenza. enhancing antibody: Ab reacts, does not neutralize and may allow virus-Ab complex to enter cells that lack virus receptor thus excasterbating disease. cytotoxic T lymphocyte/antibody dependent complement mediated cytotoxicity: destruction of virus infected cells is a problem where tissues are not regenerative, encephalitis. auto immune responses: can be due to viral protein resemblance of host protein or over stimulation of host immune response.
what are some factors that can cause differences in viral pathology in outbred (variable) populations like humans?
age (very young and very old), lifestyle (nutritional status, promiscuity, etc), immune system status leads to more serious infections and reactivtion of latent infections, genetic factors can influence the viral replicative capacity and efficacy of immune response ex if the european deletion of the AIDS receptor that can lead to slow disease or immunity
what are factors that determine if a virus can be eradicated?
limited number of serotypes, host range limited to man, effective vaccine or antiviral drug to block transmission, no long term persistence or latency,