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

HIV (human immunodeficiency virus) viraemia in serum or plasma of HIV-infected individuals was investigated by the polymerase chain reaction assay (PCR) in combination with reverse transcription to detect HIV-1 genomic RNA. Before PCR, plasma or serum was ultracentrifuged, precipitated virions were then treated with a RNase-free DNase, and a cDNA from the HIV-1 genomic RNA was synthesized. Thirty-three fresh plasma and seven sera from either HIV-1 antibody-positive individuals or patients treated with AZT were tested. Plasma from three patients were assayed 3 or 6 months apart. Twelve sera from HIV-1 antibody-negative individuals were used as negative control. PCR was performed with primers in LTR, gag and env regions: 11 of 40 samples were positive with three primer pairs, 16 with two primer pairs and 11 with only one primer pair. PCR on HIV-1 genomic cDNA was positive in 38 out of the 40 plasma or serum samples (95%), regardless of the clinical stage of the infection: HIV-1 was detected in 14 of the 15 untreated subjects and in 24 of the 25 AZT-treated patients. HIV p24 antigen was detected in the serum of 38% of subjects (15 of 40). The results suggest that this method is suitable for the detection of viral particles in plasma or serum from HIV-1-infected individuals irrespective of antiviral treatment.
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PMID:The polymerase chain reaction for the detection of HIV-1 genomic RNA in plasma from infected individuals. 171 16

An application of the polymerase chain reaction (PCR) to the direct detection of human immunodeficiency virus type 1 (HIV-1) viremia is described. The amplification of specific HIV-1 sequences of gag and env viral genes was carried out after the reverse-transcription of plasma samples (plasma RT-PCR) from seropositive subjects. The assay is faster and cheaper than detection of specific HIV-1 transcripts from peripheral blood mononuclear cells by RT-PCR. The data suggest that HIV-1 viremia is detectable by plasma RT-PCR in a large proportion of seropositive individuals.
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PMID:Detection of human immunodeficiency virus type 1 genomic RNA in plasma samples by reverse-transcription polymerase chain reaction. 171 97

Two hundred and twenty-eight blood samples from 154 HIV-seropositive subjects were investigated for the presence of HIV in peripheral blood mononuclear cells (PBMC) and plasma (without prior ultracentrifugation or filtration), using normal PBMC as the target for replication. HIV was recovered from PBMC and plasma in 80.5 and 19.5% of the patients, respectively. Plasma viraemia was significantly associated with clinical manifestations of HIV infection, indicating that HIV replication increased as disease progressed. This was confirmed by the statistically significant correlations between plasma viraemia and low CD4 cell counts (P less than 0.01) and low anti-p24 antibody titers (P less than 0.01). On patient follow-up, detection of HIV in plasma was transient. p24 antigenaemia was only detected in 13.6% of cases and was also associated with advanced clinical stages of the disease. When HIV RNA detection by polymerase chain reaction (PCR) was compared with plasma viraemia, HIV RNA was detected in plasma in all symptomatic cases and in 53.8% (seven out of 13) of asymptomatic patients [Centers for Disease Control (CDC) stages II and III], confirming that PCR was far more sensitive than plasma culture. These results indicate that cell-free virus production is associated with the clinical stage of HIV infection and may serve as a marker for disease progression. Detection of HIV RNA by PCR appears to be the most sensitive method to detect viraemia.
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PMID:Plasma viraemia as a marker of viral replication in HIV-infected individuals. 172 81

Acquired immune deficiency syndrome (AIDS) is caused by infection with the human immunodeficiency virus (HIV), a human retrovirus. The virus infects cells of the immune system by attachment of a glycoprotein viral envelope (gp 120) to a molecule expressed on human helper T cells called CD4. The fusion of the virus envelope protein to its specific receptor allows HIV to penetrate the T cell. Once inside the cell viral RNA is transcribed into double-stranded DNA by an enzyme unique to retroviruses, reverse transcriptase. The double-stranded, proviral DNA travels to the nucleus of the cell and is integrated into the infected cell's chromosomal DNA where it may remain latent for years. As a result of triggers that are poorly understood, viral replication becomes activated and proviral DNA is transcribed back into genomic RNA and RNA that is translated into viral proteins, both of which are packaged and bud from the infected T cell as infectious virus. The viral life cycle orchestrates the natural history of clinical HIV infection. Three to four weeks following exposure to HIV there is a phase of rapid viral replication, high levels of plasma viremia, and development of a "flue like" illness. Four to six weeks after exposure, during this stage of acute infection, antibodies to HIV core (p24) and envelope (gp 160, gp 120, gp41) proteins appear. Six to eight weeks after exposure symptoms disappear and plasma viremia subsides, presumably due to clearance by the immune system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenesis and natural history of HIV infection. 175 33

This review summarizes available case reports, epidemiological series, and laboratory studies on the extent of transmission of HIV to infants by breast feeding. There have been 8 case reports of infants who became infected with HIV after birth, whose mothers seroconverted postpartum, by contaminated blood transfusions, artificial insemination, iv drug use, or sexual contact, in Australia, France, Rwanda, and Zaire. Only a minority of the breast fed children of these women seroconverted to HIV positive. It is possible that the likelihood of transmission is higher when the mother is viremia soon after contracting HIV. There are 2 small prospective studies, one of 641 Zambian women, of whom 16 became HIV positive within 1 year postpartum. 2 of 8 of their breast fed children (25%) seroconverted before 24 months of age. In another series of 212 women from Rwanda, 16 women seroconverted, and 9 infants became HIV positive, of whom only 4 were probably infected from breast milk. Laboratory evidence for transmission of HIV includes isolation of HIV from 5 milk samples in 1985, 1 report of HIV in colostrum in 1986, and 1 report of HIV documented in milk by electron microscopy in 1988. A study of breast milk using the polymerase chain reaction method showed 71% of breast milk specimens from HIV-positive women contained HIV DNA. The 5 published reports of analysis of breast milk from HIV+ women for HIV antibodies found that 33%, 50%, 92%, 100%, and 100% respectively of the milk specimens had anti-HIV antibodies. Whether these antibodies are capable of blocking transmission of HIV to infants is unknown. Research on the potential for human milk and its anti-HIV antibodies to inactivate HIV virus is needed, as is information on the natural history of HIV infection in breast feeding mothers and their infants. It is also unknown if the nutritional and immunological quality of the milk of an HIV-infected woman is impaired.
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PMID:Human milk and HIV infection: epidemiologic and laboratory data. 180 4

We analysed 127 specimens of cerebrospinal fluid (CSF) from 118 HIV-1-infected individuals at different stages of infection. Intrathecal antibody synthesis was evident in 23 samples tested and was more frequently directed against HIV than against rubella virus, herpes simplex virus, varicella zoster virus or cytomegalovirus. HIV was isolated from only 14% of the 127 CSF specimens, but from 82% of CSF-paired blood samples. HIV antigen was detected in 12% of CSF specimens and 44% of paired plasma samples. Twenty specimens analysed using the polymerase chain reaction (PCR) detected proviral DNA in 75% of CSF specimens. The low rate of virus recovery from CSF was caused by neither the freezing of specimens prior to culture nor therapy. In contrast, virus isolation from CSF was significantly associated with CSF cell count. Virus isolation and antigen detection in CSF were not correlated with either the Centers for Disease Control disease stage or the peripheral CD4+ lymphocyte count, whereas viraemia was significantly associated with a low CD4+ lymphocyte count. Moreover, virus isolation and antigen detection in CSF were not associated with symptoms of subacute HIV encephalitis, suggesting that these markers are not of potential value in the diagnosis of HIV-specific neurologic complications. The value of PCR in this field merits further investigation.
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PMID:Virological markers in the cerebrospinal fluid from HIV-1-infected individuals. 181 27

To investigate the effect of human immunodeficiency virus type 1 (HIV-1) infection on subsequent hepatitis B virus (HBV) infection, HIV antibody was sought in homosexual men who developed HBV infection during a hepatitis B vaccine trial. Among 134 unvaccinated HIV-1-negative men, 7% became HBV carriers, 64% had viremia, and 42% had clinical illness. Among vaccinated HIV-1-negative men, HBV infection severity decreased with number of vaccine doses administered. When adjusted for prior hepatitis B vaccination status, persons with HIV-1 infection preceding HBV infection had a significantly higher risk of developing HBV carriage, viremia, prolonged ALT elevation, and clinical illness. Among HIV-1-infected men, the risk of HBV carriage was increased in unvaccinated persons (21%) and those who failed to respond to vaccination (31%) and further increased in those who received vaccine doses at the time they developed new HBV infection (56%-80%), suggesting inactivated hepatitis B vaccine may temporarily impair the immune response to HBV infection in HIV-1-infected persons. HIV-1 infection was also associated with reduced alanine aminotransferase elevations during the first 36 months of follow-up of men who became HBV carriers.
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PMID:Outcome of hepatitis B virus infection in homosexual men and its relation to prior human immunodeficiency virus infection. 182 15

Efficacy of antiretroviral treatment is evaluated usually according to reduction of serious events (e.g. opportunistic infections while on therapy) and improvement of survival time. In stages of asymptomatic disease treatment trials have to cover very long time periods to fulfil these requirements. In asymptomatic stages, when viremia is commonly absent, monitoring the host's immune response is an indirect means of measuring antiviral efficacy. CD4+ lymphocyte counts are generally accepted as surrogate in all major trials. The subsets of the CD8+ compartment reflect early and late activation and cytotoxic immune response. CD38+, CD57, CD8+ HLA/DR+ subsets reflect the host's vigorous cellular immune response even in early stages. These subsets are candidate surrogate markers in early and late stages of HIV infection. On the other hand, CD3+ CD4- CD8-, CD19/20 (B lymphocytes) and CD16+ (natural killer cells) do not exhibit any properties of candidate surrogate markers. Established and experimental cellular surrogate markers are discussed including own data and a review of the literature.
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PMID:Lymphocyte subsets as surrogate markers in antiretroviral therapy. 182 74

The status of human immunodeficiency virus type 1 (HIV-1) infection at the time of transmission to sexual contacts remains poorly defined. Transmission to nonsexual household contacts has appeared to be rare. A total of 505 sexual and nonsexual contacts of HIV-1-infected hemophiliacs in 349 households was observed. At entry, 10% of 201 sexual partners were anti-HIV-1-positive. Follow-up of 151 uninfected partners during a total of 351 person-years of observation showed no sero-conversions, although there were 13 pregnancies during that period. Eighty-seven percent of the seronegative respondents to a detailed questionnaire reported unprotected sexual contact at least occasionally. Among 304 other household members, including 108 parents who helped administer clotting factor concentrates to their children, none was seropositive at entry. Follow-up of 263 showed no seroconversions during a total of 605 person-years of observation. Thus, anti-HIV-1-positive hemophiliacs transmitted to their partners earlier in their course but were not found to do so when prospectively observed. No relationship to level of viremia as indicated by CD4 count, HIV-1 p24 antigenemia, or acquired immunodeficiency syndrome was found. Anti-HIV-1-positive hemophiliacs had not transmitted to their nonsexual household contacts before study entry and did not do so subsequently, indicating that the risk from even close nonsexual contact is extremely low.
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PMID:Risk of human immunodeficiency virus type 1 infection among sexual and nonsexual household contacts of persons with congenital clotting disorders. 186 21

A prospective multicenter study was undertaken to isolate human immunodeficiency virus type 1 (HIV-1) from 45 homosexual men for a period of 30 months after seroconversion. Efficiency of HIV-1 isolation from peripheral blood mononuclear cells was relatively stable over time, ranging from 64% at the time of seroconversion to more than 82% after 18 months of seroconversion. However, Kaplan-Meier analysis of HIV-1 culture data indicates that the cumulative proportion of HIV-1 culture positivity at 3, 6, 12, and 18 months after seroconversion was 62, 65, 84, and 92%, respectively. No significant correlation was observed between the presence of HIV-1 p24 antigen in serum, or numbers of CD4+ and CD8+ blood lymphocytes, and HIV-1 isolation within this period of time. These data suggest that HIV-1 viremia in homosexual men gradually increases to almost 100% culture positivity by 18 months after seroconversion.
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PMID:Prospective multicenter study on isolation of human immunodeficiency virus type 1 from homosexual men after seroconversion. 188 32


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