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Query: UMLS:C0019693 (HIV)
 170,526 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The HIV epidemic has challenged nursing to rethink the tools it uses and to consider how traditional medical tools may be used in the assessment of nursing problems. This article presents information for the direct care nurse on laboratory tests and how they may be used to meet the traditional needs of physiologic assessment and evaluation and to develop specific nursing interventions. This articles discusses tests used for HIV infection, HIV disease progression, presence of microbiologic agents of opportunistic infections commonly associated with advanced HIV disease, and common laboratory tests and their special relevance to HIV. Nursing implications and interventions are discussed throughout the text.
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PMID:Application of laboratory diagnostics in HIV nursing. 860 86

A complex array of multiphasic and multifactorial immunopathogenic mechanisms are involved in the establishment and progression of human immunodeficiency virus (HIV) disease. After primary infection, acute viremia occurs with wide dissemination of HIV. During this early viremic phase, the virus is trapped within the processes of follicular dendritic cells in the germinal centers of lymphoid tissue. Also, during this phase of primary infection, some patients show major expansions of certain subsets of CD8+ T cells that are identified by the expression of a particular variable region of the beta chain of the T-cell receptor. These expansions are manifestations of responses to HIV that may be important in controlling the progression of HIV infection. In addition, inappropriate immune activation and elevated secretion of certain proinflammatory cytokines occur during HIV infection; these cytokines play a role in the regulation of HIV expression in the tissues. Infection of progenitor cells in bone marrow and the thymus contribute to the lack of regeneration of immunocompetent cells. Dendritic cells are involved in the initiation and propagation of HIV infection in CD4+ T cells. In studies of long-term nonprogressors - persons who have stable CD4+ T-cell counts and no HIV disease progression despite years of HIV infection - preserved lymph node architecture, low viral burden, and viral expression were found.
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PMID:Immunopathogenic mechanisms of HIV infection. 860 94

This study evaluated the efficacy of switching to didanosine in patients who were clinically or immunologically progressing despite zidovudine therapy. This multicenter, open-label study involved 400 patients with the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC), who had tolerated zidovudine for at least 12 weeks and had signs of clinical or immunological disease progression. They were randomly assigned to receive 600 mg/d of zidovudine (n=133), 500 mg/d of didanosine (n=131), or 200 mg/d of didanosine (n=136). The primary end point was a new AIDS-defining event or death. The study was prematurely terminated, after the first interim analysis, mainly owing to results of two controlled studies demonstrating that a change to didanosine was associated with an improved outcome in patients with advanced HIV-1 disease. The median duration of follow-up was 53 weeks. The primary end point rates were 41, 58, and 59 (per 100 person-years) in the didanosine 500 mg, didanosine 200 mg, and zidovudine groups (zidovudine vs. didanosine 500 mg, relative risk 1.28, 95% confidence interval, 0.88-1.86, p = 0.19; didanosine 200 vs. 500 mg, relative risk 1.24, 95% confidence interval, 0.85-1.79, p = 0.26). In subjects with a baseline CD4 count of 100/mm3 or more, the primary end point rates were 8, 29, and 25 (per 100 person-years) in the didanosine 500 mg, didanosine 200 mg, and zidovudine groups, respectively (zidovudine vs. didanosine 500 mg, relative risk 2.96, 95% confidence interval 0.91-9.62, p = 0.07). No difference was seen in survival. In the didanosine 500 mg group, more patients had a 50% increase in CD4 cells (10% vs. 1% in zidovudine group, p = 0.01) and an increase of > or = 2.5 kg in body weight (2% versus 3%). Fatal pancreatitis developed in one patient assigned to didanosine 500 mg and in one to zidovudine. Our data suggest that switching from zidovudine to currently recommended doses of didanosine in subjects with ARC or AIDS who show evidence of clinical and laboratory disease progression can be associated with improvements in clinical outcome as well as in surrogate markers of HIV disease progression. This effect tended to be greater among individuals with higher CD4 counts (>100/mm3).
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PMID:Switching from zidovudine to didanosine in patients with symptomatic HIV infection and disease progression. ddI Iberian Study Group. 867 28

In a clinical trial involving asymptomatic, HIV-seropositive subjects treated with either the HIV-1 immunogen (an inactivated, gp120-depleted HIV-1 virus in incomplete Freund's adjuvant) or an adjuvant control, we examined the relationship between changes in the percentage of CD4 cells over time and early clinical markers of HIV disease progression. Subjects who had an early clinical event were more likely to have a greater decline in the percentage of CD4 cells than those subjects who did not have a clinical event (p = 0.054). The greatest decline in CD4 percentage occurred within 10 weeks prior to a clinical event (mean 11% decrease from baseline). Subjects from the quartile with the greatest decline in CD4 percentage had a fivefold greater risk of having a clinical event than subjects from the quartile with the second largest decline (p = 0.045). These results demonstrate a relationship between changes in the percentage of CD4 cells and early clinical events. Further validation of this association may be useful in clinical monitoring and in evaluating therapies to treat HIV infection.
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PMID:Early clinical markers and CD4 percentage in subjects with human immunodeficiency virus infection. 867 44

Within the context of HIV disease, a marker may be described as a consequence of disease that varies over time but does not necessarily predict future disease course. To date, the most powerful marker of HIV disease progression is the CD4 cell count. Other immunologic markers include neopterin, beta 2-microglobulin, and total and HIV-specific immunoglobulin levels. Further research, which focuses on cell-mediated factors such as interleukins, tumour necrosis factor, natural killer cell activity and apoptosis, is required. Measures of viral burden, such as p24 antigenemia and proviral DNA or RNA, may also offer additional prognostic information. As methods involving quantitative polymerase chain reaction become more refined, it is hoped that they may soon be applied to the clinical setting. Clinical markers of interest include the appearance of minor opportunistic infections and the occurrence of acute retroviral syndrome, which may indicate a faster disease course. Although population-based studies have identified a number of HIV disease markers, further research is required to generalize these findings to the individual level.
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PMID:A decade of research on the natural history of HIV infection: Part 1. Markers. 869 70

Cofactors of HIV disease may be considered risk modifiers that are causally related to future disease course. The search for potential cofactors, of viral, host or environmental origin, may provide avenues for altering the natural history of HIV infection. Potential viral cofactors include viral strains, such as syncytium-inducing and nonsyncytium-inducing variants, and strains that are resistant to specific antiretroviral therapies. Although there is strong evidence that sexually transmitted diseases that lead to genital ulcers or abrasions are important cofactors of HIV transmission, their role as cofactors in HIV disease progression is less clear. Further study of agents such as human herpesviruses 6 and 8 and hepatitis C may shed light on the role of other infectious agents in progressive HIV disease. Far less research has been conducted on behavioural, genetic and sociodemographic factors that may influence HIV disease progression rates. Since current anti-HIV therapies do not offer a cure, but only a means of prolonging life, the identification of possible cofactors is critical.
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PMID:A decade of research on the natural history of HIV infection: Part 2. Cofactors. 869 71

To investigate the association of antigen specific CD4 T cell activation with HIV disease progression and AIDS-related central nervous system damage, T cell proliferation responses to HIV, CMV, and HSV were evaluated in infected individuals. CD4 T cell loss and neurocognitive impairment were assessed at 6-mo intervals. Individuals with known times of seroconversion who responded to more HIV peptides were at greater risk of progressing to < 200 CD4 T cells (P = 0.04) and dying (P = 0.03) than those with responses to fewer peptides. A positive correlation (0.52) was seen between the breadth of the HIV proliferation response and HIV plasma RNA levels. Higher proliferation responses to CMV and HSV were also associated with more rapid CD4 loss (P = 0.05). HLA phenotyped individuals (n = 150) with two HLA-DR alleles associated with response to more HIV peptides and CMV (DR-2,5,w6,10) were less likely to develop neurocognitive (P = 0.002) and neurologic impairment (P = 0.04), but were not protected from CD4 loss and death. Thus, the ability to generate a greater T cell proliferation response to HIV and opportunistic herpes viruses may lead to resistance to central nervous system damage, but also risk of more rapid HIV disease progression.
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PMID:Pathogenic and protective correlates of T cell proliferation in AIDS. HNRC Group. HIV Neurobehavioral Research Center. 869 65

As the 21st century approaches and the proportion of the US population over 65 years of age increases, it is expected that the demand for long-term care will expand dramatically. This expectation has been widely discussed. Less widely discussed is a potential for increase in the demand for long-term care resulting, not from the geriatric conditions with which the industry is already familiar, but from chronic and debilitating substance abuse-related diseases. In the United States, the incidence of severe cardiovascular and hepatological deterioration in younger patients has begun to increase, partly due to the increased scope of drug use and the increased variety of drugs used by individuals under the age of 35. HIV disease progression resembles these degenerative conditions in some important ways, and HIV infection is now often accompanied by substance abuse disorders. Thus, the care of HIV-infected patients can serve as a model for the impact on the long-term care industry that this new type of patient is likely to make. Using HIV as a particularly dramatic example, this paper discuss those changes in detail, and concludes with recommendations for successfully adapting to them.
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PMID:Drug abuse, AIDS, and the coming crisis in long-term care. 870 75

Twenty-nine gay men (20 HIV+, 9 HIV-) received daily massages for one month. A subset of 11 of the HIV+ subjects served as a within subject control group (one month with and without massages). Major immune findings for the effects of the month of massage included a significant increase in Natural Killer Cell number, Natural Killer Cell Cytotoxicity, soluble CD8, and the cytotoxic subset of CD8 cells. There were no changes in HIV disease progression markers (CD4, CD4/CD8 ratio, Beta-2 microglobulin, neopterin). Major neuroendocrine findings, measured via 24 hour urines included a significant decrease in cortisol, and nonsignificant trends toward decrease of catecholamines. There were also significant decreases in anxiety and increases in relaxation which were significantly correlated with increases in NK cell number. Thus, there appears to be an increase in cytotoxic capacity associated with massage. Implications for HIV+ men as those with other illnesses, particularly cancer, are discussed.
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PMID:Massage therapy is associated with enhancement of the immune system's cytotoxic capacity. 870 83

Exceptionally potent cytotoxic T lymphocyte responses are generated after HIV invasion and probably control the primary infection as well as the asymptomatic phase of HIV infection. The chronic phase appears as a quasi-equilibrium between waves of new HIV variants and variant-specific CTLs, thus sustaining continuous CTL activation which eventually fails to eradicate HIV disease progression and the reascension of viral replication. Meanwhile, both the host and the virus develop various strategies either to stop or to evade this potentially deleterious permanent CTL activity. The transient effectiveness of CTLs opens perspectives for understanding disease progression generally as well as for immune therapeutic strategies.
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PMID:Evolution and plasticity of CTL responses against HIV. 879 18


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