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Videx® 742 viral hemagglutination
and vaccine development is progressing. Mucosal immunity
is mediated by secretory IgA antibodies necessary for
protection. V. cholerae is noninvasive, thus antibodies block
adherence and inhibit colonization. They neutralize the
toxin or inhibit binding to specific receptors. The intestinal
immune response begins in lymphoid follicles where
mononuclear cells are responsible for phagocytic uptake of
antigen from the intestine. Live microorganisms are more
effective immunogens than killed ones. An initial infection
with cholera yields long-lasting immunity. The most
important protective agent is the O antigen of lipopolysaccharide
(LPS). Antibodies to TCP are protective but are
biotype-restricted as a consequence of biotype-specific
antigenic variation in the major structural subunit. The
other protective antigen is the B subunit of CT. The major
epidemic strain now appears to be 0139, which increases
the significance of anti-LPS immunity; this new strain has
the virulence of the original 01 El Tor strains. Immunity
against non-LPS antigens is far less important than to a
specific LPS type. Non-LPS antigens are less immunogenic
than the LPS antigen.
Videx ®
A synthetic purine nucleoside analogue approved by the
FDA to treat human immunodeficiency virus (HIV). The
mechanism of action includes the activation of didanosine
to dideoxyadenosine 5′-triphosphate, which inhibits the
activity of HIV-1 reverse transcriptase by competing with
the natural substrate and by incorporation into viral DNA.
Didanosine is the active component.
Vif (HIV)
A protein of human immunodeficiency virus that stabilizes
recently synthesized HIV DNA and aids its passage to the
nucleus. It inhibits CEM-15 packaging into virions.
vimentin
A 55-kDa intermediate filament protein synthesized by
mesenchyma cells such as vascular endothelial cells,
smooth muscle cells, histiocytes, lymphocytes, fibroblasts,
melanocytes, osteocytes, chondrocytes, astrocytes, and
occasional ependymal and glomerular cells. Malignant
cells may express more than one intermediate filament. For
example, immunoperoxidase staining may reveal vimentin
and cytokeratin in breast, lung, kidney, or endometrial
adenocarcinomas.
vinblastine
A chemotherapeutic alkaloid that leads to lysis of rapidly
dividing cells by disruption of mitotic spindle microtubules.
It is used to treat leukemia, Hodgkin disease, lymphoproliferative
disorders, and malignancies.
vincristine
A chemotherapeutic alkaloid that lyses proliferating cells
via disruption of mitotic spindles. It is used to treat leukemia
and other malignancies.
vinyl chloride (VC)
A synthetic resin that represents a toxin of immunologic
significance in occupational exposure. It is associated
with mixed connective tissue disease. Autoantibodies are
formed against ribonucleoproteins (RPs). Human leukocyte
antigen (HLA) disease association studies have implicated
HLA-DR5 of haplotype A1B8 and HLA-DR3 with these
syndromes. Oxidized metabolites of VC are highly reactive
and bind to sulfhydryl groups, amino radicals, and
nucleotides. VC can induce oxidative cell injury and may
enhance the immunogenicity of self molecules. Oxidizing
agents may inactivate T suppressor cells. Cell surface thiols
influence the activities of lymphocytes. The reduction of
disulfide bridges to thiols is linked to increased cellular
activity. By contrast, thiol oxidation to disulfides decreases
cell responsiveness. CD8 + T cells are more sensitive to thiol
blockers and oxidants than CD4 + T cells. Exposure to VC,
mercury, iodides, and toxic oils may pose interactions with
cellular thiols, leading to preferential inactivation of CD8 +
T suppressor cells.
Viracept ®
An inhibitor of the human immunodeficiency virus 1
(HIV-1) protease that prevents cleavage of the gag–pol
polyprotein, resulting in the production of noninfectious
virus. The FDA has approved it for the treatment of HIV.
Nelfinavir mesylate is the active component.
Capsid
Nucleic acid
Viral capsids.
Capsomere
viral capsids
Envelope antigens that inhibit adherence and invasion of
host cells. Antibodies may also act as opsonins that increase
the attractiveness of viral particles to phagocytic cells.
Secretory IgA antibody is important in neutralizing viruses
on mucosal surfaces. Complement also facilitates phagocytosis
and may be significant in viral lysis.
viral hemagglutination
Selected viruses may combine with specific receptors
on surfaces of red cells from various species to produce
hemagglutination. The ability of antiviral antibodies to
inhibit this reaction constitutes hemagglutination inhibition,
which serves as an assay to quantify the antibodies. One
must be certain that inhibition is due to the antibody and
not to nonspecific agents such as mucoproteins with myxoviruses
or lipoproteins with arborviruses. Blood sera to be
assayed by this technique must have the inhibitor activity
removed by treatment with neuraminidase or acetone
extraction, depending on the chemical nature of the inhibitor.
The attachment of virus particles to cells is termed
hemadsorption. Among viruses causing hemagglutination
are those that induce influenza and parainfluenza, mumps,
Newcastle disease, smallpox and vaccinia, measles, St.
Louis encephalitis, western equine encephalitis, Japanese
B encephalitis, Venezuelan equine encephalitis, West Nile
fever, dengue viruses, respiratory syncytial virus, and some
enteroviruses. Herpes simplex virus can be absorbed to
tanned sheep red cells and hemagglutinated in the presence
of specific antiserum against the virus. This method is
termed indirect virus hemagglutination.