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cytokine synthesis inhibitory factor 210 cytomegalovirus (CMV) immunity<br />

Cytokine/receptor complex.<br />

Cytokine/receptor complex.<br />

cytokine synthesis inhibitory factor<br />

Refer to interleukin-10.<br />

cytokine upregulation of HIV coreceptors<br />

HIV-1 virus strains use the chemokine receptors, CCR-5,<br />

CXCR-4, or both, to enter cells. Expression of these<br />

chemokine receptors may predetermine susceptibility of<br />

hematopoietic subsets to HIV-1 infection. Certain cytokines<br />

can influence the dynamics of HIV-1 infection by altering<br />

chemokine receptor expression levels on hematopoietic<br />

cells. During chronic HIV-1 infection, proinflammatory<br />

cytokines such as TNF-α and IFN-γ are secreted in excess.<br />

IFN-γ increases cell surface expression of CCR-5 by human<br />

mononuclear phagocytes and of CXCR-4 by primary<br />

hematopoietic cells. In addition, GM-CSF can decrease and<br />

IL10 can increase expression of CCR-5. Further research<br />

into cytokine-mediated regulation of chemokine receptors<br />

may lead to increased understanding of how these receptors<br />

affect the pathogenesis of AIDS.<br />

cytolysin<br />

A substance such as perforin that lyses cells.<br />

cytolytic<br />

An adjective describing the property of disrupting a cell.<br />

cytolytic reaction<br />

Cell destruction produced by antibody and complement or<br />

perforin released from cytotoxic T lymphocytes.<br />

cytolytic T lymphocytes (CTLs)<br />

Effector T cells that identify and fatally injure target<br />

cells exhibiting foreign peptide complexed to MHC class<br />

I molecules. Cytotoxic cytokines increased in perforin/<br />

granzyme-mediated cytotoxicity represent mechanisms of<br />

target cell death.<br />

cytomegalovirus (CMV)<br />

A herpes (DNA) virus group that is distributed worldwide<br />

and usually is not a problem, except in individuals who<br />

are immunocompromised, such as the recipients of organ<br />

or bone marrow transplants and individuals with acquired<br />

immune deficiency syndrome (AIDS). Histopathologically,<br />

typical inclusion bodies that resemble an owl’s eye are<br />

found in multiple tissues. CMV is transmitted in the blood.<br />

Two classes of antiviral drugs are used to treat human<br />

immunodeficiency virus (HIV) infection and AIDS.<br />

Nucleotide analogs that inhibit reverse transcriptase activity<br />

include azidothymidine (AZT) dideoxyinosine and<br />

dideoxycytidine. These analogs may diminish plasma HIV<br />

RNA levels for considerable periods but often fail to stop<br />

disease progression because of the development of mutated<br />

forms of reverse transcriptase that resist these drugs. Viral<br />

protease inhibitors are now used to block the processing<br />

of precursor proteins into mature viral capsid and core<br />

proteins. Currently, a triple-drug therapy consisting of<br />

protease inhibitors is used to reduce plasma viral RNA to<br />

very low levels in patients treated for more than one year. It<br />

remains to be determined whether resistance to this therapy<br />

will develop. Disadvantages include their great expense<br />

and the complexity of their administration. Antibiotics are<br />

used to treat the many infections to which AIDS patients<br />

are susceptible. Viral resistance to protease inhibitors may<br />

develop after a few days, but resistance to the reverse transcriptase<br />

inhibitor zidovudine may only occur after months<br />

of administration. Three of four mutations in the viral<br />

resistance to zidovudine yet only one mutation can lead to<br />

resistance to protease inhibitors.<br />

cytomegalovirus immune globulin intravenous<br />

(human, injection)<br />

Indicated for prophylaxis of cytomegalovirus disease associated<br />

with transplantation of kidney, lung, liver, pancreas,<br />

and heart. Also used to prevent or attenuate primary CMV<br />

disease in immunosuppressed recipients of organ and bone<br />

marrow transplants.<br />

cytomegalovirus (CMV) immunity<br />

Cytomegalovirus that induces injury only if the host<br />

immune response is impaired, which makes it a significant<br />

pathogen for fetuses, allograft recipients, and individuals<br />

with acquired immune deficiency syndrome (AIDS).<br />

Host immune response to CMV is both cell-mediated<br />

and humoral. Cytotoxic T lymphocytes are specific for<br />

viral structural phosphoproteins. Cell-mediated immunity<br />

appears to be the major mechanism that controls CMV replication<br />

in murine CMV; however, natural killer (NK) cells<br />

are also important. Viral proteins induce a limited humoral

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