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Evolution of the V3 envelope domain in proviral sequences and isolates of human immunodeficiency virus type 1 during transition of the viral biological phenotype.
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Beyond the male condom: the evolution of gender-specific HIV interventions for women.
As the number of HIV infections in women has increased, there has been a concomitant recognition that prevention efforts to reduce sexual transmission must address the gendered context in which risk behavior occurs. This paper provides a longitudinal perspective on the emergence of the HIV epidemic in U.S. women and the parallel development of interventions to reduce risk. In the first portion of this paper, we briefly discuss the growth of the epidemic among women and how public health responses reflected the early discourse about infected women. We also address methods of protection available to women, and the emerging recognition of the importance of gender relations. In the second half of this paper, we show how gender-specificity in prevention efforts has evolved, using a framework developed by Geeta Gupta (2001) and relying on published reviews of the intervention literature in the past 10 years. Finally, we discuss in detail several recent examples. We conclude with a discussion of future directions.
[Evolution of the seroprevalence of HIV-1 and HIV-2 infections in the national hospital of Niamey, Niger].
For 25,368 serologies examined in the biological laboratory of National Hospital of Niamey, Niger, from March 1987 to May 1990, the authors studied seroprevalence HIV1, HIV2 and HIV1 + HIV2 during this periode in the different groups studied: Blood donors, in women patients of child bearing age, pregnant women, prostitutes, prisoners and during systematic visits. It appears there is a tendancy of an increase in HIV1, a decrease in HIV2 and relative stability for the two profiles together.
[Progression of viral infection in twins born from a mother infected with human immunodeficiency virus].
We studied the evolution of HIV-1 infection and immune response during six years in two twins born from an infected mother. The children had a continuous progression of the infection, proved by CD4+ cell count, serum anti-HIV antibodies, cultivable virus and proviral load. Now, both children are on antiviral treatment. The analysis of serum antibodies showed a different immune response in both children. One of them developed higher levels of antibodies directed against viral proteins and synthetic peptides derived from their aminoacid sequence. In this child, the amount of cultivable virus increased less than in his twin. Nucleotide sequencing of a part of viral genoma, showed that the virus belonged to the B subtype, prevalent in America and Europe. The observed differences in viral sequences suggest a different selective pressure in both twins. This phenomenon could be related to the observed differences in immune response.
Decreased HIV transmission after a policy of providing free access to highly active antiretroviral therapy in Taiwan.
BACKGROUND: Taiwan established a nationwide surveillance system for human immunodeficiency virus (HIV) infection in 1989 and adopted a policy to provide all HIV-infected citizens with free access to highly active antiretroviral therapy (HAART) beginning in April 1997. This provided an opportunity to determine the effect of the widespread use of HAART on the evolution of the HIV epidemic. METHODS: We analyzed national HIV surveillance data. The HIV transmission rate was estimated by use of an exponential model of HIV epidemic evolution, with statistical projection over the interval between infection and detection to fit the surveillance data. RESULTS: By the end of 2002, the cumulative number of HIV-infected citizens in Taiwan had reached 4390 (0.019% of the total population). After free access to HAART was established, the estimated HIV transmission rate decreased by 53% (0.391 vs. 0.184 new cases/prevalent case-year [95% confidence interval, 31%-65%]). There was no statistically significant change in the incidence of syphilis, in the general population or among HIV-positive patients, during the same period. CONCLUSION: Providing free HAART to all HIV-infected citizens was associated with a 53% decrease in the HIV transmission rate and contributed to the control of the HIV epidemic in Taiwan.
Are smear-positive pulmonary tuberculosis patients a 'sentinel' population for the HIV epidemic in Cameroon?
OBJECTIVE: To assess whether the human immunodeficiency virus (HIV) seroprevalence rate in adults with smear-positive pulmonary tuberculosis (PTB) can serve as a sentinel group for the estimation of HIV prevalence in the general adult population in Cameroon. DESIGN AND METHODS: A systematic review of reported HIV seroprevalence rates in the general adult population and in adults aged 15 years and over with PTB in Cameroon, using indexed and non indexed articles, publications, and reports from 1989 to 2000. Reconstruction of the evolution of the HIV seroprevalence in the two populations was done, and the relationship between these was established by the regression equation and the calculation of the correlation coefficient r. RESULTS: During the period 1989-2000, the evolution of HIV seroprevalence in the general adult population and in adults with PTB showed a steady increase, with a strong linear relationship (r = 0.96, df 7, P < 0.01). Each percentage increase of HIV seroprevalence among PTB patients corresponded to an increase of seroprevalence of about 0.3% in the general population. CONCLUSIONS: HIV seroprevalence in PTB patients in Cameroon could serve as a 'sentinel' for HIV seroprevalence in the general population.
[Evolution of CD4 and CD8 lymphocyte subsets in HIV seronegative and seropositive hemophiliacs].
PURPOSE: To asses the evolution over time of the CD4, CD8 and total lymphocyte counts in both HIV seronegative and HIV seropositive haemophiliacs. PATIENTS AND METHODS: A total of 124 haemophilic patients (77 HIV seropositive and 47 HIV seronegative) regularly controlled at our Hospital were studied. All patients have had several (range 2-15) CD4 and CD8 lymphocyte counts, with a minimum interval of 2 or more years between the first count and the last one (median 7.7 years). A linear regression analysis of the serial cell counts against the time was made and the corresponding slopes were estimated for each patient and expressed as a percentage of the initial values (standardized slopes). RESULTS: In HIV seronegative patients the number of CD4, CD8 and total lymphocytes decreased (p < 0.05), but the decrease of the CD4/CD8 ratio was not statistically significant. The decline of the CD4 cells showed a trend to remain above 500 cells/microL. HIV seropositive hemophiliacs had also a substantial decline of lymphocyte counts (p < 0.0001), but essentially due to changes of the CD4 cells, which declined with a nearly constant rate during the follow-up (median values decreased from 793/microL to 324/microL). CD8 cell counts diminished in lower grade than the CD4 cells counts, and consequently the percentage of the total lymphocyte number increased from 42% to 55%. The CD4/CD8 ratio decreased with a standardized slope of -5.7% per year. At the initial evaluation the seropositive patients had CD4 cell counts and CD4/CD8 ratios lower than seronegative ones, but CD8 cell counts were higher in the first group. Total lymphocyte counts were not statistically different at this first evaluation between infected and non-infected patients. At the final evaluation, differences on CD4 cell counts and CD4/CD8 ratio increased, and lymphocyte counts were significantly lower in the HIV-seropositive haemophiliacs. However, the final absolute counts of CD8 cells were not dissimilar in the two groups of patients. The median standardized slopes of the total lymphocyte counts, CD4 cell counts, and CD4/CD8 ratios were significantly more negative for the HIV-infected patients (-5.7%, -9.4 and -5.7%, respectively) than were these for the non-infected ones (-2.0%, -3.2% and -2.5%, respectively). CONCLUSIONS: Lymphocyte counts, mainly the CD4 cell counts, decline in treated haemophiliacs independently of their HIV status. In the HIV seronegative patients the CD4 cell counts generally stabilize above 500 cells/microL. However, in the seropositive haemophiliacs these counts show a continuous fall, with a median rate of 9% of the initial value per year.
The origins of acquired immune deficiency syndrome viruses: where and when?
In the absence of direct epidemiological evidence, molecular evolutionary studies of primate lentiviruses provide the most definitive information about the origins of human immunodeficiency virus (HIV)-1 and HIV-2. Related lentiviruses have been found infecting numerous species of primates in sub-Saharan Africa. The only species naturally infected with viruses closely related to HIV-2 is the sooty mangabey (Cercocebus atys) from western Africa, the region where HIV-2 is known to be endemic. Similarly, the only viruses very closely related to HIV-1 have been isolated from chimpanzees (Pan troglodytes), and in particular those from western equatorial Africa, again coinciding with the region that appears to be the hearth of the HIV-1 pandemic. HIV-1 and HIV-2 have each arisen several times: in the case of HIV-1, the three groups (M, N and O) are the result of independent cross-species transmission events. Consistent with the phylogenetic position of a 'fossil' virus from 1959, molecular clock analyses using realistic models of HIV-1 sequence evolution place the last common ancestor of the M group prior to 1940, and several lines of evidence indicate that the jump from chimpanzees to humans occurred before then. Both the inferred geographical origin of HIV-1 and the timing of the cross-species transmission are inconsistent with the suggestion that oral polio vaccines, putatively contaminated with viruses from chimpanzees in eastern equatorial Africa in the late 1950s, could be responsible for the origin of acquired immune deficiency syndrome.
Stable antenatal HIV-1 seroprevalence with high population mobility and marked seroprevalence variation among sentinel sites within Nairobi, Kenya.
OBJECTIVES: To monitor and analyse trends in HIV-1 seroprevalence among antenatal women in Nairobi, Kenya. DESIGN: Six sequential surveys were carried out among antenatal clinic attenders at four Nairobi City Council health centres between November 1991 and April 1997. METHODS: A total of 6828 women attending for first antenatal clinic visit were administered a standard questionnaire to obtain demographic information and were screened for HIV-1. RESULTS: HIV-1 seroprevalence rose from 12.1% in the first survey to 16.2% in the third, completed in October 1993. No rise was observed in subsequent surveys, and seroprevalence among women under the age of 20 declined after the third survey. Significant differences in seroprevalence (P < 0.001) were observed in all survey rounds between women who reported that their province of origin was Nyanza (22.4% overall), compared with those from other provinces in western Kenya (14.1%), and the eastern group of provinces (8.9%). The rise in HIV-1 seroprevalence observed between 1991 and 1993 was almost entirely attributable to the rising seroprevalence among women from Nyanza. There were considerable differences in HIV-1 seroprevalence among the four health centres, partly accounted for by differences in the proportion of clinic attenders from different provinces of origin, which also changed significantly over time. CONCLUSIONS: HIV-1 seroprevalence has stabilized in antenatal women attending these health centres in Nairobi, and may be declining among women in the youngest age group. This may reflect stabilization of HIV-1 incidence, but further observation is required. The levels of infection among Nairobi residents reflect the evolution of the HIV epidemic in their provinces of origin, and changing client composition influences HIV-1 seroprevalence at different clinics. HIV sentinel surveillance should be carried out at multiple sites in large urban centres to monitor accurately the evolution of the HIV epidemic and the impact of control efforts in reducing transmission.
Re: Follow-up study of intrahost HIV type 2 variability reveals discontinuous evolution of C2V3 sequences.
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A genetic-algorithm approach to simulating human immunodeficiency virus evolution reveals the strong impact of multiply infected cells and recombination.
It has been previously shown that the majority of human immunodeficiency virus type 1 (HIV-1)-infected splenocytes can harbour multiple, divergent proviruses with a copy number ranging from one to eight. This implies that, besides point mutations, recombination should be considered as an important mechanism in the evolution of HIV within an infected host. To explore in detail the possible contributions of multi-infection and recombination to HIV evolution, the effects of major microscopic parameters of HIV replication (i.e. the point-mutation rate, the crossover number, the recombination rate and the provirus copy number) on macroscopic characteristics (such as the Hamming distance and the abundance of n-point mutants) have been simulated in silico. Simulations predict that multiple provirus copies per infected cell and recombination act in synergy to speed up the development of sequence diversity. Point mutations can be fixed for some time without fitness selection. The time needed for the selection of multiple mutations with increased fitness is highly variable, supporting the view that stochastic processes may contribute substantially to the kinetics of HIV variation in vivo.
Evolution of human immunodeficiency virus type 1 (HIV-1) resistance mutations in nonnucleoside reverse transcriptase inhibitors (NNRTIs) in HIV-1-infected patients switched to antiretroviral therapy without NNRTIs.
We studied the evolution of nonnucleoside reverse transcriptase inhibitor (NNRTI) resistance mutations among 29 human immunodeficiency virus type 1 (HIV-1)-infected patients who experienced virologic failure when receiving an NNRTI-containing regimen (nevirapine, delavirdine, or efavirenz) and subsequently switched to antiretroviral therapy without NNRTIs. Genotypic resistance was determined from plasma samples collected at the time of NNRTI withdrawal (baseline) and during follow-up. At baseline, 83% of patients had more than two thymidine analog resistance mutations (TAMs), and all had NNRTI resistance mutations. Mutations at codons 103, 181, and 190 were found in 62, 62, and 34% of the patients, respectively. Follow-up samples were available after a median time of 6 months in all patients and at 12 months in 22 patients. The mean number of resistance mutations to NNRTIs was significantly lower at months 6 (1.34 +/- 1.04) and 12 (1.18 +/- 1.05) than at month 0 (2.03 +/- 1.02) (P < 0.009). The percentages of patients with at least one NNRTI resistance mutation were 100, 76, and 73% at baseline, month 6, and month 12, respectively (P < 0.0044). Overall, 70% of the patients had a mutation at codon 103 or 181 at month 12. The mean number of TAMs did not vary significantly during follow-up. Our data show that, in the context of maintained antiretroviral therapy, NNRTI resistance mutations persist in two-thirds of the patients in spite of NNRTI withdrawal. These results argue for the low impact of NNRTI resistance mutations on viral fitness and suggest that resistance mutations to different classes of drugs are associated on the same genome, at least in some of the resistant strains.
An application of population genetic theory to synonymous gene sequence evolution in the human immunodeficiency virus (HIV).
A population genetic model is developed and then applied to the synonymous gene sequence variation observed in samples of the Human Immunodeficiency Virus Type 1 (HIV-1). The samples, which were taken from several previous studies, contain sequences of the envelope glycoprotein gene (gp 120) of HIV-1. This analysis suggests that the viral population within an infected patient at any specific time is likely to be composed of close relatives. The viruses in a sample are likely to share a recent common ancestor probably due to consistent positive selection for non-synonymous mutations coupled with low recombination in this region of the genome. There is no substantial difference in synonymous evolutionary rate between samples of sequences obtained from Peripheral Blood Mononucleate Cells (PBMCs) and samples taken from blood plasma. This is likely to be due to the high rate of migration between these 2 HIV subpopulations. The mutation rate for the genetic region examined is estimated at 9.20 x 10(-4) per site per month. Under the assumptions of the estimation procedure, this estimate can be bounded between 8.50 and 9.91 x 10(-4) with 95% confidence. When coupled with direct estimates of mutation rate, the rate of synonymous evolution suggests that the mean number of generations per month for HIV-1 in vivo is between 1 and 4.
CD4-independent infection of human B cells with HIV type 1: detection of unintegrated viral DNA.
Although B lymphocytes are a major constituent of lymphoid organs and acquire a significantly altered phenotype and function in HIV-infected individuals, it remains unclear whether CD4-negative B cells are a susceptible host for viral entry and long-term productive infection. We screened a number of Epstein-Barr virus (EBV)-positive and-negative Burkitt's lymphoma (BL) B cell lines as well as subpopulations of normal B cells that include tonsillar naive and germinal center/memory B cells for the expression of HIV-1 receptors CD4, CXCR4, and CCR5. Cell lines and resting or activated normal B cells lacked CD4 and CCR5 but expressed CXCR4. We demonstrate HIV-1 infection of a CD4-negative, EBV-negative (BL) cell line, CA46, which remained productively infected yet noncytopathic for more than 36 months in culture. HIV-1 (HTLV-III(B)) infection of CA46 cells was mediated through CXCR4 in a CD4-independent manner and correlated with upregulation of the expression of B cell activation markers CD23 and CD95 (Fas receptor). Despite Fas receptor expression, HIV-1-infected CA46 cells remained resistant to Fas-mediated cell death. CA46-derived, CD4-independent viral isolates were proficient in infecting and causing syncytium formation in Molt4 T cells. The HIV-1 genomic organization in persistently infected CA46 clones was found to be predominantly unintegrated linear and circular DNA. Importantly, naive and germinal center/memory B cells could also be infected by HIV-1 in a CD4-independent manner. Although these B cell subpopulations expressed moderate to high levels of CXCR4, they required activation through CD40 and interleukin 4 receptor for infection. These findings point to B cells as an additional HIV-1 target and suggest a structural evolution of the HIV-1 genome responsible for CD4-independent and noncytopathic infections.
Acute human immunodeficiency virus infection temporally associated with rhabdomyolysis, acute renal failure, and nephrosis.
A previously healthy 29-year-old homosexual man presented with a 4-day history of fever, malaise, sore throat, and bleeding gums. Rhabdomyolysis, acute renal failure, and nephrotic range proteinuria were also present. The patient was found to have acute human immunodeficiency virus (HIV) infection confirmed by the presence of HIV antigen in his serum and subsequent evolution of an HIV antibody profile typical of acute seroconversion. A kidney biopsy revealed acute tubular necrosis and mesangioproliferative glomerulonephritis, with tubuloreticular inclusions. In the presence of otherwise unexplained acute renal failure, rhabdomyolysis, or new onset nephrotic syndrome, acute HIV infection should be considered in the differential diagnosis.
Body composition and nutritional parameters in HIV and AIDS patients.
Undernutrition is a frequent complication of evolutive and chronic HIV (human immunodeficiency virus) infection characterized by bodyweight loss and changes in body composition. The Centers for Disease Control and Prevention define AIDS wasting as involuntary loss of more than 10% of body weight, plus more than 30 days of either diarrhea, or weakness and fever. Wasting syndrome has been considered as a case definition of the AIDS disease since 1987. Wasting syndrome is clearly linked to disease progression and death. Despite the progress under the era of highly active antiretroviral therapy (HAART), wasting is still a problem for people with AIDS. A small part of the weight lost is fat. More important is the loss of "lean body mass", which is mostly muscle. Body composition changes during HIV infection are different from those observed in food deprivation. Under the era of HAART, a HIV-associated adipose redistribution syndrome (HARS) was described that associates subcutaneous lipoatrophy and abdominal obesity linked to various metabolic disorders. Several factors contribute to wasting syndrome. Not only low food intake and poor nutrient absorption, but mainly altered metabolism (increased resting energy expenditure) and specific disturbances in protein turnover, which is also increased. Nutritional evaluation of HIV-infected patients should include the measurement of body composition and analysis of nutritional parameters, including albumin, transthyretin and C-reactive protein. Transthyretin seems to be particularly useful to follow the recovery period of malnutrition.
[Nutritional status of the HIV patient. Description and clinical course of a group of patients over a year].
GOAL: To know the nutritional and immunological status of a sample of patients infected by HIV and their evolution over a one-year period. Relationship between nutritional status, immunological status and clinical evolution. METHOD: Longitudinal descriptive study of 30 HIV-infected patients. Anthropometric evaluation (weight, height, skin folds, arm circumference) and immunological assessment (CD4 and CD4/CD8). STATISTICAL ANALYSIS: means, absolute and relative frequencies, Student's T test. RESULTS: 30 patients, 73.3% males and 27.7% female. Mean age 34.7 years. Initial nutritional assessment: 30% of patients had normal weight, 36.7% presented mild undernourishment, 16.7% moderate undernourishment, 6.7% were overweight and 10% were obese. The evolution of CD4 and CD4/CD8 levels was not significantly influenced by nutritional status. CONCLUSIONS: The patients in the study presented a deterioration of their nutritional status, as assessed by triceps skin fold. The nutritional status of the HIV-infected patients in our study is not dependent on their immunological status. The diagnosis and treatment of their de-nourishment on diagnosis of HIV infection will contribute to the prevention of complications, thus reducing the human and health-care costs. An increase in food intake, on its own, does not improve the condition of the patients, indicating the need to provide them with the necessary dietary supplements from the early stages of illness.