Mycobacterium genavense infection and survival.
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AIDS-Related Opportunistic Infections↗
Biomedical subjects
D R Hoover
Publications and source records attributed to D R Hoover.
Evaluation of secular trends in CD4+ lymphocyte loss among human immunodeficiency virus type 1 (HIV-1)-infected men with known dates of seroconversion.
The rate at which immunodeficiency develops in untreated human immunodeficiency virus type 1(HIV-1)-infected persons might be increasing or decreasing over time because of viral evolution or other factors. Beginning in 1984, Multicenter AIDS Cohort Study investigators recruited HIV-1-seronegative homosexual/bisexual men from four US metropolitan areas and examined them semiannually for HIV-1 seroconversion. To assess possible secular changes in the natural history of HIV-1 infection, the authors examined CD4+ lymphocyte data from 354 men who seroconverted between 1984 and 1991. To control for measurement differences among centers and over time, the authors adjusted CD4+ lymphocyte values to those of persistently seronegative participants. CD4+ lymphocyte percentage measurements at the first seropositive visit formed a U-shaped pattern, with the lowest values observed in 1988 and 1989. The authors observed no consistent secular pattern of CD4+ percentages at later visit dates, except that mean CD4+ percentages were consistently lowest in men who seroconverted in 1988. In a proportional hazards model, the time to the adjusted CD4+ lymphocyte count of < 500 cells/mm3 was not associated with the secular time of seroconversion (relative hazard = 1.05, 95% confidence interval 0.97-1.13). The authors' data do not suggest a major change in the natural history of HIV-1 infection of this population.
Acquired Immunodeficiency Syndrome↗
Predictors for failure of Pneumocystis carinii pneumonia prophylaxis. Multicenter AIDS Cohort Study.
OBJECTIVE: To identify clinical and epidemiological factors associated with failure of Pneumocystis carinii pneumonia (PCP) prophylaxis in those receiving primary and secondary prophylaxis. DESIGN: Longitudinal cohort study of participants infected with human immunodeficiency virus type 1 in the Multicenter AIDS Cohort Study who used PCP prophylaxis regimens after their T-helper lymphocyte counts had decreased to less than 0.200 x 10(9)/L (200/microL). MAIN OUTCOME MEASURE: Occurrence or recurrence of PCP. RESULTS: A total of 476 participants reported taking one or more of the following regimens: trimethoprim-sulfamethoxazole (TMP-SMX), dapsone, and/or aerosolized pentamidine--367 as primary prophylaxis and 109 as secondary prophylaxis after a previous episode of PCP. A total of 92 (20%) developed PCP despite prophylaxis. The mean failure rates per person-year of follow-up were 16.0% for those receiving primary prophylaxis and 12.1% for those receiving secondary prophylaxis (P = .19). Median times to death after initiation of primary or secondary prophylaxis were 2.0 and 1.2 years, respectively. The main predictor for failure of PCP prophylaxis was profound T-helper lymphocytopenia; 86% of failures occurred after T-helper cell counts decreased to less than 0.075 x 10(9)/L and 76% occurred after counts decreased to less than 0.050 x 10(9)/L. In multivariate time-dependent analysis, when compared with counts between 0.100 x 10(9)/L and 0.200 x 10(9)/L, the risk ratio for failure with counts less than 0.050 x 10(9)/L was 2.90 (P < .001). Once T-helper cell counts were considered, fever was the only other health status indicator that predicted subsequent PCP (ie, a time-dependent risk ratio of 2.22; P = .01). Use of TMP-SMX as the prophylaxis regimen was protective but did not eliminate failure (ie, a time-dependent risk ratio of 0.55; P = .03). CONCLUSIONS: These findings strongly support identifying improved methods of PCP prophylaxis once T-helper cell counts decrease to less than 0.075 x 10(9)/L or 0.100 x 10(9)/L. Given this severe degree of immunosuppression, an inherently more effective regimen against P carinii is required.
AIDS-Related Opportunistic Infections↗
Changes in serum lipoprotein(a) in hyperlipidemic subjects undergoing long-term treatment with lipid-lowering drugs.
Though the exact physiology and pathology of lipoprotein(a) [Lp(a)] remains unknown, it has been demonstrated that increased serum Lp(a) levels are correlated with an increased risk of atherosclerotic vascular disease. The effects of lipid-lowering drugs on Lp(a) levels is unclear because of inconsistencies between study designs. This study analyzes the effects of the commonly used lipid-lowering drugs pravastatin (PRAV), lovastatin (LOV), and cholestyramine (CHOL) on serum Lp(a) and other serum lipid levels in a parallel study design. Hyperlipidemic men (n = 32) were enrolled from three centers and treated for 48 weeks in a multicenter clinical trial using PRAV, LOV, CHOL, or a placebo (for the first 16 weeks only). Baseline serum low-density lipoproteins (LDL-C), high-density lipoproteins (HDL-C), and triglycerides were 199 +/- 38, 40 +/- 9, and 160 +/- 70 mg/dl, respectively. At the end of 48 weeks, serum plasma LDL-C declined in patients randomized to PRAV, LOV, and CHOL, respectively, by 31%, 29%, and 23% (all p < 0.001); HDL increased by 4%, 11%, and 11% (all p < 0.001); and TG changed by -16%, -28%, and +43% (all p < 0.001). Subjects in PRAV and LOV changed Lp(a) by 9% and 3%, respectively. Although there was an initial Lp(a) decline in the first 8 weeks of CHOL therapy (p < 0.05, ANOVA), this returned to baseline after 48 weeks. In this parallel study design PRAV, LOV, and CHOL are effective LDL-lowering medications with minimal effects on plasma Lp(a).
Adult↗
Problems in interpreting HIV sentinel seroprevalence studies.
Estimating human immunodeficiency virus (HIV) prevalence from sentinel seroprevalence studies is difficult. We characterize these studies and show that most are investigations of incompletely defined (hypothetical) cohorts and are usually based on nonprobability samples. Prevalence in HIV sentinel serosurveys is also time-averaged and vulnerable to several time-dependent sources of bias (e.g., migration, deaths, and changes in incidence). Assumptions must be made that these time-dependent biases did not meaningfully affect the data, and this can be helped by reducing the period of investigation. Furthermore, we show that "reliability" can not be adequately measured by standard error, that "internal validity" is vulnerable to self-selection bias and laboratory problems, and that "generalizability" is limited. We propose that what is needed is a procedure (like formal metaanalysis methods) incorporating information from several separate HIV sentinel seroprevalence studies, in a manner that is reproducible and can take into consideration the differences between studies.
Acquired Immunodeficiency Syndrome↗
An epidemiologic analysis of Mycobacterium avium complex disease in homosexual men infected with human immunodeficiency virus type 1.
Cofactors associated with the Mycobacterium avium complex (MAC) disease and its prognosis in incident cases of AIDS in homosexuals were studied. We compared 51 men in whom MAC disease developed as the initial AIDS-defining illness (termed AIDS illness hereafter); 157 men who had MAC disease subsequent to another AIDS illness; and 884 men who had only non-MAC AIDS illnesses. MAC disease was the initially diagnosed AIDS illness more often in Baltimore (6.9%) and Los Angeles (5.6%) than in Chicago (2.6%) and Pittsburgh (0) (P < .01). MAC disease also was a more common subsequent AIDS illness in Baltimore (14.3%) and Los Angeles (22.4%) than in Chicago (8.5%) and Pittsburgh (6.5%) (P < .0001). Prophylaxis for Pneumocystis carinii infection increased the occurrence of MAC disease as the initial AIDS illness (from 2.3% to 12.5%; P < .0001). A low white blood cell (WBC) count was slightly more predictive of MAC disease than was a low CD4+ cell count. At 0-6, 7-12, and 13-18 months before diagnosis, the WBC cell counts of 75.0%, 61.1%, and 50.0%, respectively, of those with MAC disease as the initial AIDS illness were < or = 3,400/microL. Men in whom cytomegalovirus disease developed were at higher risk for subsequent MAC disease (relative hazard = 2.65; P < .0001). MAC disease also increased the risk for subsequent cytomegalovirus disease (relative hazard = 3.96; P < .0001).
AIDS-Related Opportunistic Infections↗
Infant mortality and maternal vitamin A deficiency during human immunodeficiency virus infection.
The maternal factors that contribute to high mortality rates among infants born to women with human immunodeficiency virus (HIV) are unclear. We followed 474 HIV-infected mothers and their infants in Malawi from pregnancy through the infants' 12th month of life. Of the 474 HIV-infected pregnant women, 300 (63.3%) were deficient in vitamin A (serum level of vitamin A, <1.05 micromol/L). Mean serum vitamin A levels among mothers whose infants died were 0.78 +/- 0.03 micromol/L compared with 1.02 +/- 0.02 micromol/L among mothers whose infants had survived for the first 12 months of life (P <.0001). The overall infant mortality rate was 28.7%. We divided HIV-positive mothers into six groups according to serum vitamin A levels (micromol/L) as follows: group 1, <0.35; group 2, between 0.35 and 0.70; group 3, between 0.70 and 1.05; group 4, between 1.05 and 1.40; group 5, between 1.40 and 1.75; and group 6, >1.75. Infant mortality rates for each group were 93.3%, 41.6%, 23.4%, 18.5%, 17.7%, and 14.2%, respectively (P < .0001). Maternal vitamin A deficiency during HIV infection may contribute to increased infant mortality.
Adult↗
The effect of human immunodeficiency virus infection on birthweight, and infant and child mortality in urban Malawi.
BACKGROUND: Low birthweight, prematurity and intra-uterine growth retardation (IUGR) are major determinants of child survival. Therefore, it is important to assess excess mortality due to human immunodeficiency virus (HIV) infection in populations where low birthweight is common. METHODS: A prospective study was conducted on 1385 children born to seropositive and seronegative women in urban Malawi. Children were regularly examined and tested for HIV. RESULTS: The mortality rate of children of HIV seropositive mothers was substantially higher (223/1000 at 12 months, 317/1000 at 24 months and 360/1000 at 30 months) than that of children of seronegative mothers (68/1000 at 12 months, 106/1000 at 24 months and 118/1000 at 30 months). The incidence of prematurity and IUGR was also higher in infants of HIV seropositive mothers than in infants of seronegative mothers (12.7% versus 3.8%, P < 0.001 for premature and 7.7% versus 4.4%, P = 0.02 for IUGR infants). The mother-to-infant HIV-1 transmission rate was 35.1%. After 12 months of age, HIV infected children showed the highest mortality; however, uninfected children of HIV seropositive and children of HIV seronegative mothers had similar mortality. The mean birthweight of HIV infected and uninfected children was not significantly different. In HIV infected children the most frequent causes of death were diarrhoea, pneumonia and failure to thrive. Less common risk factors for child mortality included active maternal syphilis and cervicitis/vaginitis. CONCLUSION: The substantial difference in survival among children of HIV infected and uninfected mothers suggests that mortality could be reduced if HIV infection were not a risk factor. To decrease childhood mortality, a combination of interventions such as treatment of sexually transmitted infections during pregnancy and measures to reduce mother-to-infant transmission should be adopted.
Birth Weight↗
Prognostic factors in human immunodeficiency virus-positive patients with a CD4+ lymphocyte count < 50/microL.
This analysis investigated variability of survival time in a cohort of 553 human immunodeficiency virus type 1 (HIV-1)-infected homosexual or bisexual men with < 50 CD4+ cells/microL. Median survival after the first CD4+ cell count < 50/microL was 1.34 years; 25% survived > or = 2 years. Multivariate analysis showed longer survival with concurrent acyclovir and zidovudine use, hemoglobin > or = 12 g/dL, and full-time employment (P < .0001). Other significant covariates associated with longer survival included African-American race, no prior AIDS illness, weight loss < 4.5 kg, and zidovudine use (with or without concurrent acyclovir) after CD4+ cells fell to < 50/microL. An easily derived score identified Multicenter AIDS Cohort Study subjects likely to survive > 2 years after CD4+ cell count was < 50/microL. Survival once CD4+ cell count fell below 50/microL may be longer for persons with a good performance status and specific clinical markers. Health care providers should consider these variables in decision-making strategies and design of clinical trials.
Acyclovir↗
The effects of long term zidovudine therapy and Pneumocystis carinii prophylaxis on HIV disease. A review of the literature.
Two lines of attack have been used against HIV-1 disease: (1) antiretroviral therapy (notably zidovudine) directed against the HIV-1 virus; and (2) chemoprophylaxis against end-stage diseases of HIV-1 infection, most notably against Pneumocystis carinii pneumonia. Many studies and clinical trials have found that zidovudine and P. carinii prophylaxis each significantly reduce short term morbidity and mortality from HIV-1 disease. However, these drugs have costs, adverse effects and (particularly with zidovudine) cumulative toxicity that suggest that their long term benefits may not necessarily be as great as their short term prospects. Due to the pressing needs of the HIV-1 epidemic, social considerations and proven short term benefits, long term clinical trials of zidovudine and P. carinii prophylaxis employing untreated control groups are impossible. Thus, the long term benefits of these anti-AIDS therapies must be estimated from observational studies comparing those who choose to use those therapies and those who do not. Strong epidemiological biases and common statistical misanalyses of observational data occur, leading to seemingly contradictory results. On the basis of the aggregate of short term clinical data and long term observational studies, zidovudine therapy taken either before or after AIDS delays the date of death by 12 months. If zidovudine therapy is initiated before AIDS, it may delay the date of diagnosis of AIDS by 12 months. However, issues of cost effectiveness, detrimental effects and optimal time to begin zidovudine therapy remain unresolved. Limited observational study data suggest that P. carinii prophylaxis initiated before the onset of clinical AIDS will delay both the date of diagnosis of AIDS and the date of death by 9 months in North American men. The net benefits from P. carinii prophylaxis will be less in those who begin this treatment after a diagnosis of AIDS. Benefits from P. carinii prophylaxis will also probably be less in regions outside of North America, in particular underdeveloped countries, where P. carinii pneumonia is less common as an end-stage HIV-1-related illness.
Acquired Immunodeficiency Syndrome↗
Long-term survival without clinical AIDS after CD4+ cell counts fall below 200 x 10(6)/l.
OBJECTIVE: Quantify and study cofactors of long-term survival without AIDS in HIV-1-infected individuals with CD4+ cell counts < 200 x 10(6)/l. DESIGN: Comparison of 579 participants who could be longitudinally evaluated for at least 3 years after the earliest date of first reaching a CD4+ cell count < 200 x 10(6)/l or an AIDS-defining illness (1987 Centers for Disease Control and Prevention definition). SETTING: Ongoing 9-year cohort study with data collected at 6-month intervals. PATIENTS: HIV-1-infected homosexual men. MEASUREMENTS AND MAIN RESULTS: Of the men, 20% did not develop an AIDS illness within 3 years following a confirmed CD4+ cell count < 200 x 10(6)/l; 29 and 28% were diagnosed with a first clinical AIDS illness from 1-3 and < 1 years, respectively, beyond their first CD4+ cell count < 200 x 10(6)/l; 23% were diagnosed with a clinical AIDS illness prior to their first CD4+ cell count < 200 x 10(6)/l. Slower decline of CD4+ cell count (P < 0.001) and presence of higher body-mass index during the period prior to the first CD4+ cell count < 200 x 10(6)/l (P < 0.001) predicted longer time to an AIDS illness once this threshold was reached. Most men had rapid loss of CD4+ cells, total T cells, and hemoglobin during the period after CD4+ cells declined below 200 x 10(6)/l. However, those remaining free of AIDS illnesses the longest arrested their decline in CD4+ cell counts and hemoglobin levels and increased total T cells during this period. Although antiretroviral therapy and Pneumocystis carinii prophylaxis extend AIDS-free survival, 45% of the group who were AIDS-free > or = 3 years after CD4+ cells fell below 200 x 10(6)/l had not used these treatments. CONCLUSIONS: Significant numbers of individuals remain free of illnesses and AIDS symptoms > or = 3 years after CD4+ cell counts drop below 200 x 10(6)/l. This occurs even in the absence of treatment. The associations seen here suggest that host and viral factors play important roles. Thus, further studies are needed to determine the biological basis of long-term survival without AIDS illnesses in HIV-1-immunosuppressed patients.
Acquired Immunodeficiency Syndrome↗
Re: "Are female smokers at higher risk for lung cancer than male smokers? A case-control analysis by histologic type".
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Case-Control Studies↗
The effect of the interaction of acyclovir with zidovudine on progression to AIDS and survival. Analysis of data in the Multicenter AIDS Cohort Study.
OBJECTIVE: To examine the effect of acyclovir use on disease progression and survival in human immunodeficiency virus (HIV)-seropositive persons treated with zidovudine. SETTING: Four university-based or -affiliated clinics. DESIGN: Prospective cohort study of homosexual and bisexual men with semi-annual follow-up. Intent-to-treat Cox models were fit to determine the relation between the use of acyclovir (modeled as a time-dependent covariate) and disease progression, controlling for baseline and time-dependent clinical and laboratory prognostic variables. The acquired immunodeficiency syndrome (AIDS)-free duration and survival time were calculated from the first use of zidovudine. Analysis included study visits 7 to 17 (from 1987 to 1992). PATIENTS: 786 HIV-seropositive participants in the Multicenter AIDS Cohort Study who began zidovudine therapy before a clinical diagnosis of AIDS; of these, 515 subsequently received acyclovir. Participants were asked at each visit whether they had "used any medication for health reasons not related to AIDS or if they had taken any medication to help fight AIDS or the HIV virus"; 488 patients indicated acyclovir use under either or both questions, and 242 patients indicated only the latter use. RESULTS: The use of acyclovir for any indication was not associated with an effect on progression to AIDS but was associated with a 26% decrease in the risk for death (relative hazard, 0.74; P = 0.07). The use of acyclovir for HIV infection was also not associated with an effect on progression to AIDS but was associated with a 36% decrease in the risk for death (relative hazard, 0.64; P = 0.01). To further investigate these findings, we examined dose, constancy, and timing of acyclovir use. The median daily dose of acyclovir used for HIV infection was between 600 and 800 mg. No apparent dose effect on survival was found. Longer uninterrupted use of acyclovir for any indication was associated with an 18% decrease in the risk for death for three or more consecutive visits (relative hazard, 0.82; P = 0.23), a 28% decrease for four or more consecutive visits (relative hazard, 0.72; P = 0.09), and a 7% decrease per visit based on the cumulative number of visits while the patient received acyclovir (relative hazard, 0.93 per visit increase; P = 0.03). Use of acyclovir for any indication and use of acyclovir for HIV infection were each associated with a 44% decreased probability of death if the drug was used after AIDS developed (P = 0.007 and P = 0.005, respectively) but not before. To further investigate the prolongation of survival, two landmark analyses were done. The first analysis began at a landmark of 1 year after initiation of zidovudine therapy and compared three groups of patients: those who used acyclovir at or before this landmark, those who had never started acyclovir or started the drug after the landmark, and those who had never used acyclovir. The 90% survival times were 1325, 1059, and 982 days, respectively. The second analysis began at a landmark of developing either a CD4 count less than 50 cells/microL or clinical AIDS. The 90% survival times for the three groups were 398, 261, and 176 days, respectively. CONCLUSIONS: Our analysis suggests that consistent use of acyclovir at a dose sufficient to suppress herpetic recurrences (that is, 600 to 800 mg/d) has a clinically significant effect on prolonging survival in a well-characterized cohort with extensive previous exposure to herpesvirus infections. Further clinical investigation of low-dose acyclovir with concomitant antiretroviral therapy is warranted.
Acquired Immunodeficiency Syndrome↗
Maternal vitamin A deficiency and mother-to-child transmission of HIV-1.
Studies show that around 10-40% HIV-positive women will give birth to children who are also infected. However, the risk factors for transmission from mother to child are not well understood and the effects of maternal nutritional status are unknown. We conducted a study of vitamin A status in pregnant women as a risk factor for mother-to-child transmission of HIV in Malawi. Serum vitamin A, height, weight, CD4 T-cell counts, and duration of breastfeeding were measured in 338 HIV-positive mothers whose infant's HIV serostatus was known. Mother-to-child transmission of HIV was 21.9% among mothers whose infants survived to 12 months of age. Mean vitamin A concentration in 74 mothers who transmitted HIV to their infants was lower than that in 264 mothers who did not transmit HIV to their infants (0.86 [0.03] vs 1.07 [0.02], p < 0.0001). We divided HIV positive mothers to 4 groups, those with vitamin A concentrations of less than 0.70, between 0.70 and 1.05, between 1.05 and 1.40, and greater than or equal to 1.40 mumol/L. The mother-to-child transmission rates for each group were 32.4%, 26.2%, 16.0%, and 7.2%, respectively (p < 0.0001). Maternal CD4 cell counts, CD4%, and CD4/CD8 ratio were also associated with increased mother-to-child transmission of HIV. Maternal age, body-mass index, and breastfeeding practices were not significantly associated with higher mother-to-child transmission. Our study suggests that maternal vitamin A deficiency contributes to mother-to-child transmission of HIV.
Acquired Immunodeficiency Syndrome↗
Beta 2-microglobulin and other early predictors of human immunodeficiency virus type 1-related wasting.
The objective of this study was to determine whether beta 2-microglobulin, neopterin, nutritional status, clinical status, immunosuppression, and hematologic status are predictors of human immunodeficiency virus (HIV)-related wasting and wasting syndrome. In addition, we aimed to determine which factors are early predictors and which are late predictors of wasting. For this cohort study of HIV-1-seropositive men seen semiannually from 1984 to 1991, a nested case-control design was used to analyze the predictive value of independent variables collected at baseline (first study visit for the seropositive cohort, first seropositive visit for seroconverters), 12 to 18 months prior, 6 to 12 months prior, and less than 6 months prior to the time at which case patients and control subjects were identified. Data on beta 2-microglobulin, neopterin, educational status, and diet were only available at baseline. A total of 41 case patients and 161 control subjects (n = 202) were identified. These were homosexual/bisexual men who were either HIV-seropositive on entering the study (n = 177) or who seroconverted during the study period (n = 25). Case patients were defined as men who had lost more than 10% of their baseline weight or who had a clinical diagnosis of wasting syndrome using the 1987 Centers for Disease Control definition. Control subjects had less than 5% weight loss from baseline or no weight loss at all. Four control subjects were matched to each case patient (where possible) by age and duration of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Incidence of clinical AIDS conditions in a cohort of homosexual men with CD4+ cell counts < 100/mm3. Multicenter AIDS Cohort Study.
Incidence rates of AIDS illnesses are described among patients with < or = 100 CD4 cells/mm3 grouped by use of antiretrovirals and chemoprophylaxis. Data were obtained from 2646 homosexual men infected with human immunodeficiency virus type 1. Participants were in the Multicenter AIDS Cohort Study during 1985-1993. The incidence rates per 100 person-years for Pneumocystis carinii pneumonia were 47.4 without treatment, 21.5 with antiretrovirals alone, and 12.8 with antiretrovirals combined with chemoprophylaxis. For Kaposi's sarcoma these rates were 23.2, 11.3, and 15.1, respectively. The incidence of some opportunistic infections, including Mycobacterium avium complex, nonretinitis cytomegalovirus disease, and cytomegalovirus retinitis, increased among persons receiving P. carinii pneumonia prophylaxis, because of reduction of this pneumonia and extension of life span. The incidence pattern of AIDS-defining illnesses in patients receiving treatment points to the changing AIDS epidemic and the need for new therapies. The data are particularly relevant to the development and planning of clinical trials and to health care providers.
AIDS-Related Opportunistic Infections↗
Nonidentified responses in a proportional hazards setting.
Nonidentified response (NR), an important form of nonindependent censoring, is modelled in a proportional hazards setting. Methods to test for existence of and identify NR censored observations are developed. Incorporation of NR censoring information into appropriate algorithms can improve parameter and underlying baseline hazard estimation. Application to estimating time until death from AIDS is made.
Acquired Immunodeficiency Syndrome↗
Resistance to HIV-1 infection. Multicenter AIDS Cohort Study.
Men from the Multicenter AIDS Cohort Study were classified as "susceptible" and "resistant" to HIV infection. Resistant men were still HIV antibody negative in 1993 and were estimated to have had > 45 different anal intercourse partners (median, 92; range, 46-504) in the 2.5 years before visit 2 (1985). Susceptible men were seroconverters who were estimated to have had < 13 different anal partners (median, 4; range, 0-12). Leukocyte groups were compared between the two groups of men. Values were excluded for 12 months before the first antibody-positive visit in the susceptible men. White blood cells, polymorphonuclear neutrophils, total lymphocyte count, CD8+ percentage and number, and CD3+ and CD4+ number were higher in the resistant men. Logistic regression analyses were used to develop 50 bivariate models. Higher levels of neutrophils and CD8+ cells were included in four of the six best-fitting bivariate models, suggesting that each is associated with resistance to HIV-1 infection. These results support the hypothesis that CD8+ cells may modulate the outcome of HIV-1 exposure.
CD8-Positive T-Lymphocytes↗