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PubMed1997

Vertical HIV-1 transmission correlates with a high maternal viral load at delivery.

Transmission of HIV-1 from an infected mother to her child occurs in around 20% of cases. Although maternal, immunological, and virological factors have been implicated in transmission, clear association is not yet well defined. For this reason, we have conducted a study to determine the relative contribution of the above-mentioned factors with special emphasis on quantitative viral load. We studied 67 HIV-1-infected mothers during pregnancy and labor and their 69 newborns (two sets of twins) from two university hospitals in Barcelona. Plasma and cell samples were collected at delivery between January 1992 and May 1994, and HIV-1 RNA and p24 in plasma, CD4 cell counts, and tissue culture infectious doses (TCID) were measured. Diagnosis of infection in children was based on persistence of anti-HIV-1 antibodies at 18 months of age, a positive HIV-1 culture or polymerase chain reaction in two separate samples, or presence of signs or symptoms of AIDS before 18 months of age. Results showed a very high relationship between > 10(5)/ml viral RNA copies (odds ratio [OR] 22, 95% confidence interval [CI] 4.4-119.2, p < 0.00001), > 0.5 TCID (OR 17, 95% CI 2.1-139.7, p = 0.001), CDC B + C (OR 3.5, 95% CI 0.98-12.5, p = 0.055), < 400 CD4 cells (OR 4.1; 95% CL 1.1-15.4, p = 0.01) and transmission of HIV-1. In this study, a strong association between mother-to-child transmission of HIV-1 and a high maternal viral RNA load in plasma at delivery is demonstrated. Viral load, which is related to clinical and immunological status in the mother, is the main contributing factor for HIV-1 vertical transmission, and these findings may have global and even individual therapeutic implications.

CD4 Lymphocyte Count↗

PubMed1999

Effect of indinavir and higher CD4+ T-cell count on viral load response after 6 months of highly active antiretroviral therapy.

This retrospective, unmasked chart review was undertaken to determine which HIV-infected patients receiving protease inhibitors (PIs) for the first time were most likely to experience a decrease in plasma viral load (PVL) and which factors were associated with a PVL < 500 copies/mL below the detectable limits after 6 months. A total of 308 patients aged > 15 years with a PVL > 500 copies/mL received therapy that included a PI in addition to other antiretroviral therapies (128 patients, saquinavir hard-gel capsule 600 mg TID; 107 patients, indinavir 800 mg TID; and 73 patients, ritonavir 600 mg BID). The choice of drug was at individual clinicians' discretion. Patients were followed for a median of 10 (range, 6 to 21) months. Of the 128 patients who received saquinavir, 45% were switched to another PI (33%, indinavir; 12%, ritonavir). Seventy percent of the 73 patients initially given ritonavir were switched (45%, indinavir; 25%, saquinavir), as were 23% of the 107 patients initially given indinavir (15%, saquinavir; 8%, ritonavir). A total of 34.1% (n = 105) of patients achieved a PVL < 500 copies/mL; in 51.6%, PVL decreased > 0.5 log copies/mL. In this subgroup, both treatment-naive patients and those who were receiving a new combination of antiretroviral therapy when they started PI treatment had a more pronounced decline in PVL (P < 0.001). After adjustment by logistic regression analysis for age, sex, mode of transmission, and duration of highly active antiretroviral therapy (HAART), CD4+ cell count and initial type of PI received were independently associated with PVL < 500 copies/mL. In the present study, the treatment success rate was low (34.1%) compared with rates observed in randomized, controlled trials. A higher CD4+ cell count and use of indinavir at the initiation of HAART are associated with a better viral load response.

Adult↗

PubMed2005

Human herpesvirus 8 serological markers and viral load in patients with AIDS-associated Kaposi's sarcoma in Central African Republic.

Epidemic Kaposi's sarcoma (KS) is one of the most frequent types of cancer in several African countries; however, very few data are available on human herpesvirus 8 (HHV-8) markers in KS patients from Central Africa. In a series of 36 AIDS-KS cases from Central African Republic, we showed, using a real-time PCR quantitative assay, the high frequency (82%) of detectable HHV-8 DNA in peripheral blood mononuclear cells (PBMCs). We also found that the level of antibodies directed against lytic or latent HHV-8 antigens is not correlated to the amount of HHV-8 viral load in the PBMCs, and finally, we demonstrated a much higher viral load in tumoral skin lesions (6.07 log copies/mug DNA) than in unaffected skin (2.93 log copies/mug DNA) or in PBMCs (2.55 log copies/mug DNA).

AIDS-Related Opportunistic Infections↗

PubMed2005

Viral coinfection in the oral cavity of HIV-infected children: relation among HIV viral load, CD4+ T lymphocyte count and detection of EBV, CMV and HSV.

Viral coinfection in the oral cavity associated to HIV infection was evaluated in 180 children from birth to 13 years of age of both sexes. The oral examinations were performed at the Pediatric AIDS Outpatient Clinic, São Lucas Hospital and Clinic Hospital, both in Porto Alegre, Brazil and at the School of Dental Medicine, University Hospital Center, State University of New York at Stony Brook, USA. The aim of this study was to identify the presence of viral infections in the oral cavity. PCR technique was used to determine opportunistic viral infections caused by CMV, EBV, and HSV in mucosal swabs. A high frequency of viral infection was detected in the oral cavity of HIV-infected children determined by the PCR technique. HIV-infected children with viruses had a favorable CD4+ T lymphocyte count and unfavorable viral load.

AIDS-Related Opportunistic Infections↗

PubMed1998

The effectiveness of combined saquinavir and ketoconazole treatment in reducing HIV viral load.

With the advent of protease inhibitors, the treatment of persons infected with the human immunodeficiency virus (HIV) has resulted in lower levels of the virus in the blood. The first of these protease inhibitors was saquinavir, which inhibits the HIV protease enzyme responsible for post-translational processing of Gag and Gag-Po1 poly protein precursors into their functional products. Studies have suggested that ketoconazole, given in combination with saquinavir, increases the bioavailability of saquinavir. This study compared the HIV viral load in patients treated with saquinavir alone and in combination with ketoconazole. Results showed that while all patients who received saquinavir exhibited a positive response, patients who also received ketoconazole had a greater drop in viral load levels. In addition, a greater number of patients had undetectable viral levels after 3 months on the ketoconazole/saquinavir regimen. These results indicate that the combination of saquinavir/ketoconazole for the treatment of HIV requires further study.

Antifungal Agents↗

PubMed2006

Impact of chloroquine on viral load in breast milk.

The anti-malarial agent chloroquine has activity against HIV. We compared the effect of chloroquine (n = 18) to an anti-malarial agent without known anti-HIV-activity, sulfadoxine-pyrimethamine (n = 12), on breast milk HIV RNA levels among HIV-infected breastfeeding women in Zambia. After adjusting for CD4 count and plasma viral load, chloroquine was associated with a trend towards lower levels of HIV RNA in breast milk compared with sulfadoxine-pyrimethamine (P = 0.05). Higher breastmilk viral load was also observed among women receiving presumptive treatment for symptomatic malaria compared with asymptomatic controls and among controls reporting fever in the prior week. Further research is needed to determine the potential role of chloroquine in prevention of HIV transmission through breastfeeding.

Adult↗

PubMed2003

Increased proportions of activated and proliferating memory CD8+ T lymphocytes in both blood and lung are associated with blood HIV viral load.

One mechanism of HIV pathogenesis has been proposed to be the activation of T lymphocytes, resulting in proliferation and decreased survival of these activated cells. Others have suggested that co-infections may exacerbate this process. These hypotheses were tested by examining the relationship between HIV blood viral load with the proportion of activated and proliferating CD8+ lymphocytes in lung and blood. In the lung these responses were compared in patients with or without respiratory pathogens. Thirty-five HIV-positive patients and five controls underwent bronchoalveolar lavage (BAL). BAL and blood samples were fixed and permeabilized and the proportions of memory CD8+ lymphocytes that expressed the activation marker CD38 and the cell cycling marker Ki67 were measured by flow cytometry. CD38bright CD8+ lymphocytes from both sites increased with increasing blood viral load. In BAL there was no significant difference between the CD38 activation status in those with respiratory pathogens compared with those without. More CD38bright CD8+ lymphocytes expressed Ki67 when compared with the CD38dim lymphocytes. These findings provide evidence that HIV is the primary factor in stimulating CD8+ cell activation.

ADP-ribosyl Cyclase↗

PubMed1999

Lymphocytic alveolitis, bronchoalveolar lavage viral load, and outcome in human immunodeficiency virus infection.

Lymphocytic alveolitis portends a poor prognosis in human immunodeficiency virus (HIV)-infected subjects. Because alveolar lymphocytes consist predominantly of HIV-specific CD8(+) cytotoxic T lymphocytes (CTL), they could represent an appropriate immune response to infected cells in the lung, and be a surrogate marker for a high pulmonary viral burden. We assessed long-term outcome in a cohort of asymptomatic HIV-infected subjects who underwent bronchoscopy between 1990 and 1993 and had bronchoalveolar lavage fluid (BALF) available for determination of viral load by reverse transcription-polymerase chain reaction. The ability to detect HIV in BALF increased with disease progression. Lymphocytic alveolitis, although present at all stages of HIV infection, was most pronounced in patients with middle stage disease. The HIV viral load as measured by bronchoalveolar lavage correlated with the percentage of alveolar lymphocytes in patients with peripheral blood CD4(+) cell counts above 200/microliter. Including patients with CD4(+) cell counts < 200/microliter weakened this correlation, possibly because of replacement of CD8(+) CTL by CD8(+) suppressor cells in advanced disease. Free virus in BALF was a stronger predictor of HIV disease progression than was lymphocytic alveolitis. These data suggest that lymphocytic alveolitis in HIV-infected subjects occurs in response to viral antigens in the lung and that the poor prognosis associated with lymphocytic alveolitis reflects a high pulmonary viral burden.

Adult↗

PubMed2002

Male viral load and heterosexual transmission of HIV-1 subtype E in northern Thailand.

We evaluated the association between HIV-1 RNA copies/mL in men and heterosexual transmission to their female partners among 493 couples in Thailand. Husbands were identified as HIV-positive when they were screened as blood donors; nearly all were infected with HIV subtype E. Wives had no known risks for HIV infection other than sex with their husbands. In multivariate analysis, each log10 increment of HIV RNA in the man was associated with an 81% increased rate of HIV transmission to his wife (odds ratio = 1.81, 95% confidence interval: 1.33-2.48). No transmission occurred at viral loads below 1094 copies/mL, and a dose-response effect was seen with increasing viral load in the man. In multivariate analysis, a history of a sexually transmitted disease in the man or woman, longer duration of hormonal contraceptive use, and the woman's onset of sexual activity at less than 20 years of age were also associated with increased seropositivity of the wife.

Adult↗

PubMed2005

Role of viral load in the pathogenesis of chicken anemia virus.

The pathogenesis of strain 3711 of the chicken anemia virus (CAV), propagated in chickens, and two preparations of strain 3711 that had been adapted to grow to high titre in cells of the MDCC-MSB1 line were studied in chicken embryos and/or chickens. Highest viral loads in infected chickens, as measured by a microplate DNA-hybridization assay, were detected in the thymus, clotted blood and pancreas, and the lowest in the duodenum. The CAV DNA copy number in the organs of chicken embryos was significantly lower than in chickens. Route of infection was an important determinant of the course of disease in chickens, with clinical signs appearing earlier in birds infected by the intramuscular than those infected by the oral route; there was a direct relationship between viral load in particular organs and the extent of clinical signs. No reduction in the pathogenicity for chickens was noted for strain 3711 after 65 or 129 passages in the MDCC-MSB1 cell line.

Animals↗

PubMed2005

Chronic herpes simplex virus type-2 infection and HIV viral load.

By December 2003, the estimated adult HIV/AIDS prevalence rate in sub-Saharan Africa was 7.5-8.5%, and rates of herpes simplex virus type-2 (HSV-2) infection among adults aged >30 years ranged from 60% to 82%. However, little is known about the natural history of HIV/HSV-2 co-infection in this population. We evaluated HIV viral load and CD4+ cell counts among persons with and without chronic HSV-2 co-infection in a cross-sectional study of HIV-infected persons not receiving antiretroviral therapy. HSV-2 and HIV co-infection was associated with a 0.3 log copies/mL higher HIV viral load compared with persons without HSV-2 infection (P=0.014). Chronic HSV-2 infection may have a negative effect on the clinical course of persons with HIV.

Adult↗

PubMed1999

Acyclovir treatment of experimentally induced herpes simplex virus encephalitis: monitoring the changes in immunologic NO synthase expression and viral load within brain tissue of SJL mice.

The effect of acyclovir treatment on viral burden and the expression of immunologic nitric oxide synthase (iNOS) within brains of 42 HSV-1 F infected mice was studied by using a titration PCR assay for HSV-1 DNA and a semiquantitative RT-PCR for iNOS mRNA. iNOS mediated NO-production may possibly be involved in secondary mechanisms of brain injury following virus infection, which may account for treatment failures in human herpes simplex virus encephalitis (HSVE). Following infection, a parallel increase of iNOS mRNA and HSV-1F-DNA occurred with peaks after 7 days that were both significantly lower under acyclovir treatment. Six months post infection viral load had declined, but iNOS mRNA expression in both treated and untreated mice was still enhanced as compared with mock infected controls. This suggests that acyclovir decreases iNOS expression via inhibition of viral replication shortly after infection but fails to influence elevated iNOS within the brain late in the course of experimental HSVE.

Acyclovir↗

PubMed2003

Effect of dexamethasone on tracheal viral load and interleukin-8 tracheal concentration in children with respiratory syncytial virus infection.

BACKGROUND: Lower respiratory tract infection caused by respiratory syncytial virus (RSV) is in part an immune-mediated disease. For that reason corticosteroids might be effective, especially in patients with severe RSV lower respiratory tract infection. Our aim was to assess the effect of dexamethasone on tracheal viral load and airway inflammation in patients with RSV infection. METHODS: Mechanically ventilated children with proven RSV infection were randomized to receive dexamethasone (0.6 mg/kg/day in four doses for 48 h) or placebo. Daily tracheal aspirates were analyzed for viral load (by quantitative polymerase chain reaction), interleukin (IL)-8 and white blood cell count. RESULTS: The RSV RNA concentrations decreased in a similar manner from baseline in the dexamethasone (9 patients) and in the placebo group (13 patients). IL-8 decreased from baseline in the dexamethasone group but increased in the placebo group during the first 48 h [change from baseline at 24 h, -2.3 vs. 0.9 ln ng/ml (95% confidence interval for difference, -4.2 to 0.3, P = 0.02) and at 48 h, -4.2 vs. 0.4 ln mg/ml (95% confidence interval for difference, -5.3 to -0.3; P = 0.03), respectively], without effect on the tracheal white blood cell count. CONCLUSION: Dexamethasone does not cause an impaired decline of tracheal RSV but lowers IL-8 of children mechanically ventilated for RSV lower respiratory tract infection, potentially leading to less inflammation and reduced phagocyte activation.

Base Sequence↗

PubMed2001

Increased soluble Fas in HIV-infected hemophilia patients with CD4+ and CD8+ cell count increases and viral load and immune complex decreases.

Previous studies interpreted increases of soluble Fas (sFas) in the plasma during disease progression in HIV-infected patients as evidence of increased apoptosis of CD4(+) lymphocytes. We studied whether sFas and sFas ligand (sFasL) plasma levels are associated with CD4(+) and CD8(+) lymphocyte counts, plasma viral load, and IgM, IgG, C3d, and gp120 complexes on circulating CD4(+) blood lymphocytes in long-term surviving HIV-infected hemophilia patients, most of whom were receiving HAART. Twenty-six hemophilia patients who were infected with HIV in the early 1980s were investigated in 1997, 1998, and 1999. HAART was initiated in 1996 and 1997 in most patients. Lymphocyte subpopulations and immune complex-coated CD4(+) lymphocytes in the blood were investigated by flow cytometry, plasma viral load (HIV-1 mRNA copies/ml plasma) was tested with HIV-1 QT Nuclisens kits, sFas (ng/ml) and sFasL (ng/ml) plasma levels were measured with MBL ELISA kits, and the in vitro response of patient lymphocytes was tested in cell cultures. During the period from 1997 to 1999 we observed an increase in sFas plasma levels (p = 0.003) as well as in CD4(+) (p = 0.004) and CD8(+) (p = 0.023) cell counts; a decrease in IgG (p = 0.047), C3d (p = 0.024), and gp120 (p = 0.001)-coated CD4(+) lymphocytes in the blood; and a decrease in the number of impaired mitogen stimulation assays (p = 0.013). sFas was negatively associated with viral burden (r = -0.662, p = 0.0002) as well as with CD4(+)IgM(+) (r = -0.554, p = 0.004), CD4(+)IgG(+) (r = -0.431, p = 0.031), CD4(+)C3d(+) (r = -0.551, p = 0.041), and CD4(+)gp120(+) (r = -0.430, p = 0.041) blood lymphocytes, CD8(+)DR(+) cell counts (r = -0.700, p = 0.016), and impaired in vitro responses of patient lymphocytes to PHA (r = -0.475, p = 0.016). sFasL was negatively associated with total lymphocyte counts (r = -0.433, p = 0.027), as well as with absolute numbers of CD3(+) (r = -0.492, p = 0.011) and CD8(+) (r = -0.432, p = 0.027) cells. We conclude that, contrary to expectations, sFas plasma levels increased in long-term surviving HIV-infected hemophilia patients receiving HAART, concomitant with increases in CD4(+) and CD8(+) cell counts. Increased sFas may reflect the growing pool of T lymphocytes that recovers because of a decreasing viral burden and a decreasing immune complex load of CD4(+) lymphocytes.

Antigen-Antibody Complex↗

PubMedDate not supplied

Decrease in viral load associated with topical dinitrochlorobenzene therapy in HIV disease.

Quantitative measurement of human immunodeficiency virus (HIV) RNA is being used to assess the efficacy of various treatment modalities in HIV disease. Topical dinitrochlorobenzene (DNCB) therapy has been associated with improved clinical and immunologic parameters in HIV-infected patients. We have now examined the effect of topical DNCB treatment on plasma HIV RNA levels in a small prospective study. Eight HIV-infected subjects had T-cell counts and plasma viral load measured prior to initiation of DNCB therapy and 3-4 months after starting treatment. Six patients who refused DNCB therapy served as simultaneous controls. The mean CD4 and CD8 T-cell counts did not change significantly in either group over the study period. In contrast, plasma HIV RNA levels decreased one-half to greater than one log in each DNCB-treated subject, and the decrease in viral copies was statistically significant (p = 0.006). In the control group, plasma HIV RNA levels increased significantly over the course of the study (p = 0.037). We conclude that topical DNCB therapy has the ability to lower viral load in HIV-infected patients. The long-term effect on viral burden of this inexpensive, readily available therapeutic modality merits further investigation.

Administration, Topical↗

PubMed1997

Apoptosis of CD4+ and CD19+ cells during human immunodeficiency virus type 1 infection--correlation with clinical progression, viral load, and loss of humoral immunity.

Enhanced rates of programmed cell death (apoptosis) have been detected in T cells and B cells from human immunodeficiency virus type 1 (HIV-1)-infected individuals. To evaluate the possible relevance of this event to HIV pathogenesis and disease progression, apoptosis in CD4+ T lymphocytes and CD19+ B lymphocytes, viral load, and neutralizing antibody titers were assayed in HIV-1-infected slow progressors and progressors. A correlation was found between progressive disease and apoptosis of CD4+ T cells. The extent of apoptosis in CD4+ cells was similar in slow progressors and seronegative control subjects. By contrast, we found elevated levels of B-cell apoptosis in all HIV-1-infected individuals compared with seronegative control subjects, with a tendency toward increased levels of apoptosis with progressive disease. Apoptosis in CD4+ T cells and CD19+ B cells correlated with viral RNA levels in plasma. Furthermore, higher rates of B-cell apoptosis were observed in individuals with poor neutralizing activity against a panel of six clinical HIV-1 isolates. From these results we conclude that the extent of apoptosis in cultured CD4+ cells and CD19+ cells appears to parallel the decline in CD4 cell counts in infected individuals. The finding of a relation between apoptosis in B cells and poor neutralizing capacity suggests that apoptosis may be related to loss of immune function. A role for apoptosis in the pathogenesis of AIDS is also supported by the strong correlation between viral load and rates of apoptosis in CD4+ T cells.

Antibody Formation↗

PubMed2003

Fluctuation of HCV viral load before seroconversion in a healthy volunteer blood donor.

BACKGROUND: Newly implemented NAT has been shown to be able to effectively identify HCV-positive blood donated during the preseroconversion period. STUDY DESIGN AND METHODS: EDTA-plasma pools of 24 donations were tested using an HIV-1/HCV multiplex NAT under an FDA-approved IND application. Samples in a positive pool were retested individually. Positive samples were further tested by two discriminatory assays to determine specific viral reactivity. Upon obtaining informed consent, seronegative donors with positive NAT results were enrolled into a follow-up study for risk factor analysis and laboratory testing. RESULTS: A donation by a 29 year old female was identified as HCV NAT-positive with negative serology and an elevated ALT. Her two previous donations, 5 and 12 months earlier, were both seronegative and with normal ALT. Her husband tested positive for HCV RNA. The donor remained seronegative for at least 36 days. The index donation had a viral RNA concentration of >500,000 copies per mL while the first seropositive sample was NAT-negative. Laboratory data on serial follow-up samples showed 100- to 1,000-fold fluctuations in viral load during a period of 48 days prior to seroconversion. CONCLUSIONS: This case suggests that, at least in some newly infected individuals, the HCV viral load can fluctuate dramatically prior to seroconversion, and that NAT, even on individual samples, will not totally prevent HCV transmission.

Adult↗

PubMed2000

Relationship of CD4+ T cell counts and HIV type 1 viral loads in untreated, infected adolescents. Adolescent Medicine HIV/AIDS Research Network.

The REACH Project (Reaching for Excellence in Adolescent Care and Health) of the Adolescent Medicine HIV/AIDS Research Network was designed as a study of an adolescent cohort composed of HIV-1-infected and -uninfected subjects. The goal of the analysis presented was to examine the relationship of CD4+ T cell counts and HIV-1 plasma viral loads in adolescents. The CD4+ T cell counts of 84 HIV+ subjects who were 13 to 19 years of age were measured at the clinical sites, using ACTG standardized techniques. HIV-1 viral loads in frozen plasma were determined by the NASBA/NucliSens assay at a central laboratory. Past and current treatment with antiretroviral drugs was determined by medical record abstraction and interview data. The slope of the line generated by regressing log10 HIV-1 RNA (copies/ml) versus CD4+ T cell counts of REACH subjects who are antiretroviral drug naive was negative and significantly different than zero. A negative association has also been reported for antiretroviral drug-naive, adult males in the Pittsburgh Men's Study, a component of MACS (Pitt-MACS) (Mellors J, et al.: Science 1996;272:1167). These data show that in adolescents, as in adults, HIV-1 RNA concentrations are correlated with corresponding absolute CD4+ T cell count. The slopes of the lines generated with data from each cohort were different (p = 0.003). In addition to age, there are sex and racial differences in the makeup of the two cohorts. Any or all of these differences may affect the slopes of the lines.

Adolescent↗