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

Cats infected with feline immunodeficiency virus (FIV) develop a disease syndrome similar to that caused by human immunodeficiency virus type 1 (HIV-1) infection in humans. HIV-1 replication has been shown to correlate with the disease stage and progression. To assess replication kinetics and disease progression in early FIV infection, we developed a quantitative competitive reverse transcriptase PCR to measure the plasma virus load at serial time points after virus exposure. We found that an early peak viremia immediately preceded the onset of acute-phase symptoms in infected cats. Plasma virus levels remained high throughout the symptomatic phase of infection, which lasted for 8 to 10 weeks, and then declined as clinical symptoms resolved; however, all cats maintained significant plasma virus titers through 36 weeks postinfection. Early peak viral replication coincided with the initial precipitous decline in circulating CD4+ T lymphocytes. These results indicate that FIV kinetics are similar to those of HIV-1 during the acute and secondary phase of infection and that the plasma FIV load correlates with the disease stage. These results serve to further develop the FIV model and to enhance its usefulness for pathogenesis, vaccine development, and therapeutic studies related to HIV.
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PMID:Longitudinal assessment of feline immunodeficiency virus kinetics in plasma by use of a quantitative competitive reverse transcriptase PCR. 753 56

A set of mutations [Ala-62-->Val(A62V), V75I, F77L, F116Y, and Q151M] in the polymerase domain of reverse transcriptase (RT) of human immunodeficiency virus type 1 (HIV-1) confers on the virus a reduced sensitivity to multiple antiretroviral dideoxynucleosides and has been seen in HIV-1 variants isolated from patients receiving combination chemotherapy with 3'-azido-3'-deoxythymidine (AZT) plus 2',3'-dideoxycytidine (ddC) or 2',3'-dideoxyinosine (ddI). The IC50 values of AZT, ddC, ddI, 2',3'-dideoxyguanosine, and 2',3'-didehydro-3'-deoxythymidine against an infectious clone constructed to include the five mutations were significantly higher than those of a wild-type infectious clone. The K1 value for AZT 5'-triphosphate determined for the virus-associated RT from a posttherapy strain was 35-fold higher than that of RT from a pretherapy strain. Detailed analysis of HIV-1 strains isolated at various times during therapy showed that the Q151M mutation developed first in vivo, at the time when the viremia level suddenly increased, followed by the F116Y and F77L mutations. All five mutations ultimately developed, and the viremia level rose even further. Analyses based on the three-dimensional structure of HIV-1 RT suggest that the positions where at least several of the five mutations occur are located in close proximity to the proposed dNTP-binding site of RT and the first nucleotide position of the single-stranded template.
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PMID:Emergence of human immunodeficiency virus type 1 variants with resistance to multiple dideoxynucleosides in patients receiving therapy with dideoxynucleosides. 753 21

To determine the frequency and significance of cytomegalovirus (CMV) viremia and viruria in HIV-positive subjects with low CD4+ lymphocyte counts but with no clinical indications for culture, we studied 100 consecutive clinically stable subjects with CD4+ cells < or = 100/microliters of blood who agreed to culture of blood and urine. Serum was tested for CMV antibody, p24 antigen, neopterin, and liver enzyme concentrations, and patients were offered funduscopic examination. Subjects' records were reviewed an average of 9.1 months after enrollment for evidence of subsequent CMV retinitis. Three of the original cohort proved ineligible because of CD4+ count > 100/microliters; CMV antibody was present in 96% of the remainder. Isolation of CMV from blood was uncommon (2 of 93 seropositive subjects) whereas viruria occurred in 51.6%; likelihood of having a positive urine culture was significantly related to the subject's absolute CD4+ lymphocyte count: 60% for those with CD4+ < or = 50/microliters, vs. 26.1% for those with CD4+ 51-100/microliters. Neither serum p24 antigen nor neopterin was predictive of CMV in urine or blood. No subjects submitting to ophthalmologic exam had unsuspected CMV retinitis. Subsequent development of retinitis correlated with CMV viruria on entry: 13.5% if urine-positive, 1.9% if negative (p = 0.029; Fisher exact test).
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PMID:Evidence of active cytomegalovirus infection in clinically stable HIV-infected individuals with CD4+ lymphocyte counts below 100/microliters of blood: features and relation to risk of subsequent CMV retinitis. 755 94

A total of 186 blood samples from 24 HIV-1 seropositive hemophiliac patients, monitored every four months for 29 months, were investigated for the presence of viral antigen in plasma. In addition, peripheral blood mononuclear cells (PBMC) were cultured for HIV-1, using normal PBMC as a target for replication. Antigenemia was detected in 51% of the patients and from PBMC in 87.5% of the patients. The incidence of HIV isolation in asymptomatic patients (42.8%) was similar to that found in symptomatic patients (51.4%). Patients with opportunistic infections had a higher incidence of lymphocytic viremia (p < 0.05). Plasma viremia was closely associated (p < 0.05) with low CD4+ counts and infection progression. The persistence of antigenemia was also a marker of a poor clinical course. In treated patients, plasma viremia was the marker that better correlated with the clinical course, and it did not appear during the first nine months of therapy. Zidovudine doses of > 500 mg/day significantly lowered the appearance of antigenemia and lymphocytic viremia (p < 0.05).
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PMID:Prospective study of antigenemia, plasma viremia and lymphocytic viremia in HIV-infected hemophiliacs. 755 28

In order to develop a successful subunit vaccine against infection with the human immunodeficiency virus (HIV), protective immune effector functions must be identified. Until now, there has been only indirect evidence that HIV-specific cytotoxic T lymphocytes (CTLs) fulfill this role. Using the macaque simian immunodeficiency virus (SIV) model, the protective potential of nef-specific CTLs, stimulated by vaccination, was examined in animals challenged with a high intravenous dose of the pathogenic simian immunodeficiency virus, SIVmac251(32H)(pJ5). An inverse correlation was found between the vaccine-induced nef-specific CTL precursor frequency and virus load measured after challenge. In addition, the early decline in viraemia, observed in both vaccinated and unvaccinated control animals was associated with the development of virus-specific CTL activity and not with the presence of virus-specific neutralizing antibodies. The results imply that vaccines that stimulate strong CTL responses could protect against HIV infection.
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PMID:Early suppression of SIV replication by CD8+ nef-specific cytotoxic T cells in vaccinated macaques. 758 89

A woman who had recently become infected with HIV-1 after sexual relations with a seropositive subject presented a rapid fall in CD4+ T lymphocytes and evolved to AIDS 13 months after primoinfection. The most plausible cause for the rapid disease progression in this patient was the observation of a viral syncytium forming phenotype. The plasmatic viremia was high throughout the follow up despite the administration of antiretroviral drugs.
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PMID:[Rapid progression to AIDS in a patient with infection from a strain of syncytium forming HIV-1]. 760 20

The typical course of HIV infection is characterized by multiple phases that occur over a period of eight to ten years. A critical event in the initial establishment of HIV infection is the localization of HIV in lymphoid organs that serve as major reservoirs for HIV and as primary sites for virus replication. Despite the fact that the majority of HIV-infected individuals do not show any clinical signs of disease activity for extended periods of time, HIV disease is active and progressive in lymphoid organs during this clinically latent period. Persistence of virus in lymphoid organs causes a chronic stimulation of the immune system that ultimately leads to destruction of the lymphoid tissue and loss of the ability to respond to HIV and/or other pathogens. Major expansions of restricted subsets of CD8+ T cells determined by the usage of certain variable domains (V) of the beta (beta) chain of the T cell receptor (TCR) occur in certain patients during primary HIV infection. These restricted expansions of CD8+ V beta subsets are oligoclonal and represent HIV-specific immune responses with cytolytic T cell activity. Although only limited numbers of patients were studied thus far, certain patterns have emerged that appear to correlate with the subsequent clinical outcome. It is conceivable that immunologic and virologic events associated with primary infection have a major impact on the ultimate course of HIV disease. Histopathologic, virologic, and immunologic studies of long-term nonprogressors (LTNP) indicate that a small proportion of patients who have been HIV-infected for approximately 10 years have normal lymph node architecture, brisk HIV-specific humoral and cellular immune responses, and high and stable CD4+ T cell counts serially determined over years. Viral burden and expression are low in these patients; however, low levels of viremia are present, and virus derived from mononuclear cells is replication competent and infectious in most patients. Studies of events associated with primary HIV infection, examination of lymphoid tissue at various stages of disease, and dissection of the immunologic and virologic components of LTNP should contribute substantially to our understanding of the pathogenesis of HIV disease.
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PMID:New concepts in the immunopathogenesis of HIV infection. 761 32

Acquired immunodeficiency syndrome was first recognized as a new disease in 1981 because of the unusual association of Kaposi's sarcoma and Pneumocystis carinii pneumonia in young men. The skin remains one of the most important clinical markers for acquired immunodeficiency syndrome, now recognized as the end stage of infection with the human immunodeficiency virus (HIV). Indeed, an urticarial viral exanthem appearing during seroconversion may allow early identification of newly infected individuals who might benefit from administration of antiviral therapy during plasma viremia. The "asymptomatic HIV infection" is often accompanied by multiple skin complaints, which commonly include xerosis, pruritus, psoriasis/seborrheic dermatitis, and pruritic papular eruptions, the cause of which remains controversial. Psoriasis and Kaposi's sarcoma lesions share features including angiogenesis, dermal dendrocytes infected with HIV, and epidermal hyperproliferation, and are manifested by mice transgenic for HIV provirus or Tat-ltr. Changes in the immune system including T-cell function, antigen response, and shifting cytokine expression as well as a propensity for autoimmune reactions must underlie the skin immunodysfunction occurring in the setting of HIV infection. One of the most unsettling controversies suggested by in vitro data is that ultraviolet light, an effective therapy for HIV-related skin disorders, may actually activate the virus.
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PMID:Human immunodeficiency virus and the skin: selected controversies. 761 89

To elucidate the functions of human immunodeficiency virus type 1 (HIV-1) genes in a nonhuman primate model, we have constructed infectious recombinant viruses (chimeras) between the pathogenic molecular clone of simian immunodeficiency virus (SIV) SIVmac239 and molecular clones of HIV-1 that differ in phenotypic properties controlled by the env gene. HIV-1SF33 is a T-cell-line-tropic virus which induces syncytia, and HIV-1SF162 is a macrophage-tropic virus that does not induce syncytia. A DNA fragment encoding tat, rev, and env (gp160) of SIVmac239 has been replaced with the counterpart genetic region of HIV-1SF33 and HIV-1SF162 to derive chimeric recombinant simian/human immunodeficiency virus (SHIV) strains SHIVSF33 and SHIVSF162, respectively. In the acute infection stage, macaques inoculated with SHIVSF33 had levels of viremia similar to macaques infected with SIVmac239, whereas virus loads were 1/10th to 1/100th those in macaques infected with SHIVSF162. Of note is the relatively small amount of virus detected in lymph nodes of SHIVSF162-infected macaques. In the chronic infection stage, macaques infected with SHIVSF33 also showed higher virus loads than macaques infected with SHIVSF162. Virus persists for over 1 year, as demonstrated by PCR for amplification of viral DNA in all animals and by virus isolation in some animals. Antiviral antibodies, including antibodies to the HIV-1 env glycoprotein (gp160), were detected; titers of antiviral antibodies were higher in macaques infected with SHIVSF33 than in macaques infected with SHIVSF162. Although virus has persisted for over 1 year after inoculation, these animals have remained healthy with no signs of immunodeficiency. These findings demonstrate the utility of the SHIV/macaque model for analyzing HIV-1 env gene functions and for evaluating vaccines based on HIV-1 env antigens.
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PMID:Persistent infection of rhesus macaques with T-cell-line-tropic and macrophage-tropic clones of simian/human immunodeficiency viruses (SHIV). 763 18

SCID mice were engrafted with human foetal liver, thymus and lung. Human cells were subsequently detected among peripheral blood leukocytes for 81% of tested animals and in tissue implants for 100% of tested animals. SCID-hu mice received intraperitoneal injections of human immunodeficiency virus type 1 (HIV1) at from 20 up to 20,000 median tissue culture infectious doses (TCID5). HIV1 infection was detected by means of cell culture and polymerase chain reaction both in blood and implants, up to 58 days after infection. The rate of infection was dependent upon the inoculated dose: the frequency of thymus infection ranged from 14% with 20-500 TCID50 up to 100% with 20,000 TCID50. HIV1 infection was detected less frequently in blood leukocytes than in thymus. Thymus virus load ranged from 40 to 50,000 HIV1 provirus copies per million cells and was not correlated with either infectious dose or viraemia. Thymus T-cell depletion was observed mainly in the CD1+4+8+ immature thymocyte compartment. The same rate of SCID-hu mouse infection was obtained using three different primary HIV1 isolates, suggesting that infection was not restricted to a few particular virus strains. The systemic infection of SCID-hu mice following intraperitoneal virus injection mimics some traits of human HIV infection and provides a promising, novel approach for future investigations in this field.
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PMID:Dose-dependent systemic human immunodeficiency virus infection of SCID-hu mice after intraperitoneal virus injection. 763 34


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