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Biomedical subjects

M Schechter

Publications and source records attributed to M Schechter.

At least 37 records · Page 2Linked to original sources
PubMed1997

HIV viral load and CD4+ lymphocyte counts in subjects coinfected with HTLV-I and HIV-1.

Reports indicate that there is a dissociation between markers of HIV disease progression and clinical stage among subjects coinfected with human T-cell lymphotropic virus type I (HTLV-I) and HIV. HTLV-I coinfection does not appear to affect HIV viral load, currently considered to be the best marker of HIV disease progression. We measured HIV RNA levels in stored serum samples from 23 subjects with coinfection and 92 subjects with HIV single infection and examined the correlation with the CD4+ lymphocyte count. Subjects were recruited from an ongoing HIV cohort study in Rio de Janeiro, Brazil. In both groups, CD4+ lymphocyte counts declined with increasing levels of HIV RNA. In a linear regression analysis adjusting for HIV RNA serum level, coinfected individuals had an estimated 78% higher CD4+ lymphocyte count than those with single infection. Simultaneous adjustment for beta2-microglobulin level increased the difference, with coinfected individuals having 146% (p = 0.005, 95% CI: 32% to 359%) higher CD4+ counts. These data suggest that the higher CD4+ lymphocyte counts associated with coinfection do not provide immunologic benefit and may reflect HTLV-I-associated nonspecific lymphocyte proliferation. The results of this and other studies suggest that the CD4+ count cutoff values used in making clinical decisions in HIV infection may not be appropriate in coinfection. As with HIV single infection, HIV virus load may be the optimal surrogate marker for subjects with coinfection.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Human T cell lymphotropic virus type I does not increase human immunodeficiency virus viral load in vivo.

Human T lymphotropic virus type I (HTLV-I) can increase human immunodeficiency virus (HIV) replication in vitro, and several studies suggest that HTLV-I accelerates the progression of HIV infection. To determine whether HTLV-I enhances HIV replication in vivo, a case-control study was done of serum HIV viral load, using polymerase chain reaction, in 23 subjects with HTLV-I/HIV coinfection and 92 control subjects with HIV single infection. The geometric mean serum RNA level was 11,482 copies/mL in the coinfected group and 13,804 in the single-infection group (P = .57), a result that did not change after adjustment for zidovudine use and CD4 cell count. Among subjects with advanced HIV infection, there was a trend toward higher viral load among singly infected subjects. HTLV-I did not appear to increase HIV plasma RNA levels in subjects with coinfection. These results do not provide a biologic basis for the hypothesis that HTLV-I accelerates the course of HIV infection.

Adult↗
PubMed1997

Detection of genetically diverse human immunodeficiency virus type 1 group M and O isolates by PCR.

A panel of 136 genetically diverse group M and 5 group O adult isolates from outside the United States and Europe were evaluated by PCR with the Roche AMPLICOR HIV-1 test, a modified version of the AMPLICOR HIV-1 test, and a new primer pair/probe system. Detection of some of these isolates was less efficient with the AMPLICOR HIV-1 test; however, the assay was significantly improved by reducing the sample input and lowering the annealing temperature. The new primer pair/probe set detected 140 of 141 isolates, including the 5 group O isolates that were not detected with either of the AMPLICOR HIV-1 test formats.

Adult↗
PubMed1997

Myelopathy among Brazilians coinfected with human T-cell lymphotropic virus type I and HIV.

OBJECTIVE: To determine whether subjects coinfected with HTLV-I and HIV have a higher frequency of myelopathy than subjects singly infected with HIV. DESIGN: A prospective, nested case-control study of HTLV-I and HIV coinfected (cases) and HIV singly infected adults (controls) participating in a prospective HIV cohort study at a university hospital outpatient HIV clinic in Rio de Janeiro, Brazil. MEASUREMENTS: Subjects were evaluated for evidence of myelopathy by a neurologist unaware of their HTLV serologic status. Patients with at least two pyramidal signs, such as paresis, hypertonicity or spasticity, hyperreflexia, clonus, diminished or absent superficial reflexes, or the presence of pathologic reflexes (e.g., Babinski or Hoffmann), were defined as having myelopathy. Myelopathy severity was quantified using the Kurtzke Functional Disability Scale (FDS); patients with FDS scores > or = 4 were considered to have significant myelopathy. Selected patients with myelopathy underwent lumbar puncture for the evaluation of intrathecal synthesis of HTLV-I antibodies. RESULTS: Of 15 coinfected subjects, 11 (73%) had evidence of myelopathy versus 10 of 62 subjects (16%) with HIV single infection (adjusted odds ratio [OR] = 13.0, p = 0.00002). When only myelopathy patients with FDS scores of > or = 2 or > or = 4 were included, the association between coinfection and the presence of myelopathy remained (OR = 7.3, p = 0.0003 for scores > or = 2; and OR = 8.9 for scores > or = 4, p = 0.04). In addition, a higher proportion of coinfected subjects had peripheral neuropathy (40%) than controls (16%) (OR = 3.5, p = 0.07). CONCLUSION: Coinfection with HTLV-I was strongly associated with myelopathy among subjects infected with HIV. The relative contribution of HTLV-I versus HIV in the pathogenesis of coinfection-associated myelopathy is not known. Coinfection may also be associated with peripheral neuropathy. Further studies are needed to elucidate the mechanisms of coinfection-associated neurologic conditions.

Adult↗
PubMed1996

HIV prevention in developed countries.

HIV prevention in developed countries is marked by impressive successes and dismal failures. The successes point the way to what works; the failures highlight obstacles that must be overcome. Successes include important behavioural changes among gay and bisexual men, antiviral use to prevent vertical transmission, and securing the safety of the blood supply. New strategies are needed to reach the residual of individuals continuing with unsafe practices (a special hazard in high-prevalence areas); to reach young people who are beginning to engage in sexual relations and injection drug use; and to overcome political opposition to prevention strategies.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Identification of single and dual infections with distinct subtypes of human immunodeficiency virus type 1 by using restriction fragment length polymorphism analysis.

The simultaneous presence of multiple HIV-1 subtypes has become common in communities with the growth of the pandemic. As a consequence, the potentiality for an increased frequency of HIV-1 mixed infections caused by viruses of distinct subtypes could be expected. Thus, there is a need to estimate the prevalence and geographic distribution of infections caused by viruses of a singular subtype as well as coinfections caused by two or more HIV-1 strains of distinct subtypes. To address this need, we have developed a genetic method based on restriction fragment length polymorphism (RFLP) to screen for these two types of infections within infected populations. In this assay, restriction enzymes may be used to predict the phylogroup of HIV-1 infected samples. A 297 bp pol fragment spanning the entire viral protease gene and a 311 bp fragment of the p24 gag region are used for this analysis. The viral regions are amplified by nested PCR using DNA templates from uncultured peripheral blood mononuclear cells (PBMC) or virus culture. Classification of HIV-1 strains to well defined subtypes B, D, F, and A/C is done by sequential endonuclease restriction analysis of a PCR amplified-protease gene followed by analysis of the p24 gag region. The electrophoretic migration patterns visualized by ethidium bromide staining or by radiolabeled probes are then determined on a 10% polyacrylamide gel. In infections caused by viruses of a singular subtype, a single restriction pattern is detected, whereas in multiple infections caused by two or more viral strains of different subtypes, the combination of different digestion patterns are observed in infected individuals. Using this methodology we have screened for genetic variations in HIV-1 proviral DNA from thirty-three Brazilian samples. Our RFLP procedure classified thirty-two samples as single infections caused by viruses of subtypes B (31) and F (1), and one sample as dual infection caused by distinct viral strains. Subsequent sequence and phylogenetic analysis of the viral protease gene in lymphocytes of all these patients confirmed our RFLP findings in single infections, and demonstrated the existence of two distinct HIV-1 strains of subtypes F and D in a patient which lymphocytes showed the simultaneous presence of two different digestion patterns. As up to now, single infections caused by subtype D variants were not identified in Brazil, our data provide the first evidence of subtype D HIV-1 in this country. Because sequencing of HIV proviral DNA is not particularly practical for large-scale molecular epidemiological studies, the protease/gag-based RFLP screening method will be useful to predict the phylogroup of HIV-1, and to identify multiple infections caused by HIV-1 strains of distinct subtypes. We believe that this information is crucial for both evaluation of the HIV-1/AIDS pandemic and intervention strategies.

Adult↗
PubMed1995

CD4+ blood lymphocytes are rapidly killed in vitro by contact with autologous human immunodeficiency virus-infected cells.

We have investigated the ability of human immunodeficiency virus (HIV)-infected cells to kill uninfected CD4+ lymphocytes. Infected peripheral blood mononuclear cells were cocultured with autologous 51Cr-labeled uninfected cells. Rapid death of the normal CD4-expressing target population was observed following a brief incubation. Death of blood CD4+ lymphocytes occurred before syncytium formation could be detected or productive viral infection established in the normal target cells. Cytolysis could not be induced by free virus, was dependent on gp120-CD4 binding, and occurred in resting, as well as activated, lymphocytes. CD8+ cells were not involved in this phenomenon, since HIV-infected CEMT4 cells (CD4+, CD8- cells) mediated the cytolysis of uninfected targets. Reciprocal isotope-labeling experiments demonstrated that infected CEMT4 cells did not die in parallel with their targets. The uninfected target cells manifested DNA fragmentation, followed by the release of the 51Cr label. Thus, in HIV patients, infected lymphocytes may cause the depletion of the much larger population of uninfected CD4+ cells without actually infecting them, by triggering an apoptotic death.

Apoptosis↗
PubMed1994

Coinfection with human T-cell lymphotropic virus type I and HIV in Brazil. Impact on markers of HIV disease progression.

OBJECTIVES: To study the effect of human T-cell lymph-tropic virus type I (HTLV-I) on markers of human immunodeficiency virus (HIV) disease progression. DESIGN: A retrospective, nested case-control study. SETTING: A university hospital outpatient HIV clinic in Rio de Janeiro, Brazil. PARTICIPANTS: Human immunodeficiency virus-seropositive adults participating in a prospective HIV cohort study. MAIN OUTCOME MEASURES: The HIV clinical stage, CD4+ lymphocyte counts, and other laboratory parameters in 27 individuals infected with HIV and HTLV-I (coinfection) and 99 age-matched, HIV-seropositive, HTLV-seronegative controls (single infection). RESULTS: Variables independently associated with coinfection included higher CD4+ lymphocyte count (odds ratio [OR], 2.3; 95% confidence limits [CL], 1.3, 4.1), higher CD4+ percentage (OR, 2.0; 95% CL, 1.3, 3.2), beta 2-microglobulin level of 254 nmol/L or more (OR, 6.8; 95% CL, 1.3, 35.4), World Health Organization stages 3 and 4 (OR, 4.4; 95% CL, 1.1, 18.0), and reporting a parenteral risk factor (OR, 7.4; 95% CL, 1.4, 38.9). When stratified by p24 antigenemia, coinfection was associated with an estimated 82% higher CD4+ lymphocyte count (P < .05). CONCLUSION: Coinfection was associated with higher CD4+ lymphocyte counts, more advanced clinical disease, and higher beta 2-microglobulin levels than HIV infection alone. The higher mean CD4+ lymphocyte count does not appear to offer immunologic benefit. Caution should be exercised when using CD4+ lymphocytes as a surrogate marker in studies of HIV infection in populations where HTLV-I is prevalent. Further studies are needed to address whether current CD4+ lymphocyte values for the initiation of antiretroviral therapy and chemoprophylaxis against opportunistic infections in HIV infection are appropriate in coinfection.

Adult↗
PubMed1994

Urinary tract infection in men with AIDS.

OBJECTIVE--To investigate whether bacteriuria and, specifically, symptomatic urinary tract infection (UTI) occur with increased frequency in men with HIV infection. METHODS--In this cross-sectional study we investigated three groups of men, aged from 18 to 50 years. Group A was composed of patients with a diagnosis of AIDS; Group B, of patients without HIV infection, and group C of patients with asymptomatic HIV infection. Patients with any known predisposing factor for UTI were excluded from the study. A clean-catch midstream urine sample was collected from each patient on the first day of hospital admission (groups A and B) or during a visit to the outpatient clinic (group C). Bacteriuria was diagnosed when > or = 100,000 colony forming units/ml, urine were grown. RESULTS--There were 415 patients, 151 in group A, 170 in group B and 94 in group C. Bacteriuria was significantly more frequently in group A (20 cases, 13.3%) than in groups B (3 cases, 1.8%, p = 0.00007) and C (3 cases, 3.2%, p = 0.009). Ten cases of bacteriuria in group A (6.6%) were symptomatic while no case of symptomatic UTI was seen in groups B (p = 0.0004) and C (p = 0.008). The frequency of UTI in homosexual men with AIDS (7 cases, 6.7%) was not significantly different from that observed in men with AIDS who denied homosexuality (3 cases, 6.5%). E coli was the predominant pathogen associated with UTI. Although adequate response to a two-week course of antibiotics was observed in most cases, an in-hospital mortality rate of 20% was found among AIDS patients with symptomatic UTI. CONCLUSIONS--In the present study, the frequency of bacteriuria and symptomatic UTI was found to be increased in men with AIDS. E coli was the predominant pathogen in these cases. These data suggest that symptomatic UTI may represent a relevant cause of morbidity for men with AIDS.

AIDS-Related Opportunistic Infections↗