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PubMed1995

Maintenance of high virus load even after seroconversion in newborn cats acutely infected with feline immunodeficiency virus.

The viral loads in adult and newborn cats have been compared following injection with feline CD4+ FeL-039 line cells acutely infected with feline immunodeficiency virus (FIV). The level of virus genome in peripheral blood mononuclear cells (PBMC) increased progressively despite seroconversion in the newborn cats, whereas the virus genome was apparently cleared after seroconversion in the adult cats. Immunohistochemical staining of thymus of the FIV-infected newborn cats showed clusters of viral antigen-positive cells. These results indicate that FIV infection of the newborn cat results in higher virus loads than infection of the adult cat. We discuss these findings in relation to FIV as a model system for studies of the infection of neonates with an immunosuppressive retrovirus.

Acute Disease↗
PubMed2003

Increased hepatitis C virus load among injection drug users infected with human immunodeficiency virus and human T lymphotropic virus type II.

Coinfection of hepatitis C virus (HCV) and human immunodeficiency virus (HIV) and/or human T-lymphotropic virus type II (HTLV-II) is common among drug users. We compared HCV RNA detection and load in a cohort of 6570 injection drug users from 9 US cities during 1987-1991. Of 385 subjects selected from 16 strata by sex, race (black or nonblack), and HIV/HTLV-II group (HIV positive [HIV(+)]/HTLV-II(+), HIV(+)/HTLV-II negative [HTLV-II(-)], HIV(-)/HTLV-II(+), and HIV(-)/HTLV-II(-)), 376 had HCV antibodies, of whom 305 had detectable HCV load. HCV RNA detection was unrelated to sex, race, and virus groups, but differed by study site. The mean HCV load was 5.4 log(10) IU/mL and was 0.24 log(10) higher in men than in women. Virus load increment with HIV or HTLV-II infection was higher among white subjects than among other subjects. Compared with HIV(-)/HTLV-II(-) subjects, virus load was 0.50, 0.22, and 0.56 log(10) higher in HIV(+)/HTLV-II(-), HIV(-)/HTLV-II(+), and HIV(+)/HTLV-II(+) subjects, respectively. HTLV-II infection significantly increased HCV load in white subjects but not in other racial groups.

Adult↗
PubMed1996

Antiretroviral monotherapy in early stage human immunodeficiency virus disease has no detectable effect on virus load in peripheral blood and lymph nodes.

Initiation of antiretroviral monotherapy early in the course of infection with human immunodeficiency virus may result in a temporary slowing in the rate of disease progression; however, little is known about the virologic effects of early therapy. Virus load was measured in peripheral blood and lymph nodes from 16 antiretroviral-naive patients with a mean CD4 T lymphocyte count of 659 cells/microliter at baseline and after 8 weeks of either no treatment or zidovudine therapy. CD4 T lymphocyte counts and all virologic parameters examined remained unchanged regardless of zidovudine treatment status. Histopathology and virus distribution within lymph nodes remained constant between baseline and week 8 in each patient, indicating that the virologic and histologic parameters examined in a single lymph node are representative of a systemic process. Early antiretroviral monotherapy with zidovudine had no effect on virologic parameters in this group of patients with relatively high CD4 T lymphocyte counts and low measures of virus load at baseline.

Adult↗
PubMed1997

Human immunodeficiency virus type 1-specific cytotoxic T lymphocytes (CTL), virus load, and CD4 T cell loss: evidence supporting a protective role for CTL in vivo.

The relationships between primary human immunodeficiency virus type 1 (HIV-1) Gag-specific cytotoxic T lymphocyte (CTL) frequency, virus load, and CD4 T cell loss were evaluated in a group of 46 HIV-1-infected persons with hemophilia. Freshly isolated peripheral blood mononuclear cells in limiting dilution assays were used to measure HIV-1 Gag-specific CTL frequencies. Concurrent measurements of virus load and lymphocyte surface markers were obtained. No correlation between Gag-specific CTL frequency and concurrent CD4 cell count was observed. A significant inverse relationship was observed between HIV-1 Gag-specific CTL frequency and provirus load as measured by polymerase chain reaction. Subjects with higher CTL frequencies were found to have more stable CD4 cell counts over time. These results provide additional evidence to support the concept that the predominant role of this virus-specific cellular immune response is to limit viral replication and CD4 cell loss in HIV-1 infection.

Adolescent↗
PubMed1994

Quantification of HIV-1 virus load under zidovudine therapy in patients with symptomatic HIV infection: relation to disease progression.

OBJECTIVE: To measure changes in HIV-1 virus load following zidovudine therapy, and to investigate the relationship between these changes and clinical progression. DESIGN: Prospective study of 18 symptomatic, zidovudine-naive patients, with CD4 count < 350 x 10(6)/l. METHODS: The following parameters were measured at each visit, before zidovudine therapy, after 1 month of therapy, and every 3 months thereafter. HIV-1 virus load in peripheral blood was determined by serum immune complex-dissociated HIV-1 p24 antigen (ICD-p24 Ag), quantitative plasma and cellular viraemia. A virologic response under zidovudine was defined as > 50% decrease in ICD-p24 Ag levels or > 1 log10 decrease in plasma or cellular viraemia titres from baseline values. CD4 and CD8 cell counts, and beta 2-microglobulin levels were also measured. Disease progression was defined as the time to a new AIDS-defining event or death. RESULTS: At enrolment, 13 out of 18 (72%) patients had positive ICD-p24 Ag and positive plasma viraemia, with a mean of 44 median tissue culture infective dose (TCID50) per ml; all patients had positive cellular viraemia with a mean TCID50 of 230 per 10(6)/l cells. Median CD4 cell count was 43 x 10(6)/l. Ten patients developed a new AIDS-defining event and eight died during a median follow-up of 15 months on zidovudine. Baseline prognostic markers for development of a new AIDS-defining event included ICD-p24 Ag, CD4 and CD8 cell counts, but only CD4 cell count remained predictive on multivariate analysis (P = 0.003). When each laboratory marker was analysed as a time-dependent covariate, only CD4 (P = 0.002) and CD8 (P = 0.001) cell counts predicted the occurrence of a new AIDS-defining event. Eight out of 13 (61.5%) patients had an ICD-p24 Ag response, and seven out of 13 (54%) a plasma viraemia response, but only cellular viraemia responders (five out of 18; 28%) had a 5.6-fold decrease in their risk of developing an AIDS-defining event (90% confidence interval, 1-33; P = 0.05). None of these markers correlated with survival. CONCLUSIONS: Plasma viraemia and ICD-p24 Ag, while providing useful short-term markers of zidovudine antiviral activity in vivo, do not correlate with disease progression in patients with advanced HIV infection. CD4 cell count remained the best initial and time-dependent predictor for development of new AIDS-defining events. Interestingly, a high CD8 cell count and a decrease in cellular viraemia titres also appear to be predictive of improved clinical outcome in this population.

Adult↗
PubMed1995

Zidovudine treatment prolongs survival and decreases virus load in the central nervous system of rhesus macaques infected perinatally with simian immunodeficiency virus.

To assess the potential therapeutic effects of zidovudine, rhesus macaques were inoculated with simian immunodeficiency virus (SIV) strain SMM/B670 at birth and infused either continuously or intermittently with zidovudine for 6-7 months. Zidovudine did not prevent infection but did significantly increase survival time, which was associated with lower serum p26 viral core antigen levels, a lower virus burden in the cerebrospinal fluid (CSF), and lower CSF quinolinic acid levels than in untreated monkeys. Two of 5 infected, untreated monkeys developed motor impairment within 6 months following infection, whereas motor impairments did not occur in infected, zidovudine-treated monkeys until after the drug was discontinued. Zidovudine treatment was well tolerated by rhesus infants with minimal, transient side effects. These results demonstrate that zidovudine treatment significantly decreases virus load within the central nervous system (CNS) and delays the onset of CNS dysfunction and immune disease in rhesus monkeys perinatally infected with SIV.

Animals↗
PubMed2001

Hepatitis C virus load is associated with human immunodeficiency virus type 1 disease progression in hemophiliacs.

Hepatitis C virus (HCV) and human immunodeficiency virus type 1 (HIV-1) coinfection is common in hemophiliacs and injection drug users. To assess the interaction between HCV load and HIV-1 disease progression, we examined 207 HIV-1/HCV-coinfected patients. Patients were followed prospectively for approximately 7 years, and annual measurements of CD4(+) cell counts and HCV and HIV-1 loads were obtained. Survival analysis was used to define the independent effects of HCV load on HIV-1 progression. After controlling for CD4(+) cell count and HIV-1 RNA level, every 10-fold increase in baseline HCV RNA was associated with a relative risk (RR) for clinical progression to acquired immunodeficiency syndrome (AIDS) of 1.66 (95% confidence interval [CI], 1.10-2.51; P=.016) and an RR for AIDS-related mortality of 1.54 (95% CI, 1.03-2.30; P=.036). These findings emphasize the need for further research regarding the use of HIV-1- and HCV-specific therapy in coinfected individuals.

Adolescent↗
PubMed1999

Cell-associated HIV-1 RNA in blood as indicator of virus load in lymph nodes. The Swiss HIV Cohort Study.

We have developed sensitive assays for viremia and cell-associated human immunodeficiency virus type 1 (HIV-1) RNA and DNA to assess the predictive value of virological parameters determined in blood for virus load in lymph nodes (LNs). Eighteen patients were included; 13 received stavudine/didanosine/hydroxyurea and 5 stavudine/didanosine, and all had viremia <500 copies/mL for >3 months. At the time of LN biopsy (median, 10 months), the median viremia was 2.09 log copies/mL (range, <0.70-3.34). Cell-associated HIV-1 RNA and DNA were detectable in blood and LNs of all patients. The median cell-associated RNA and DNA were 2.16 log copies/106 cells and 2.60 log copies/106 cells in blood versus 4.31 log RNA copies/106 cells and 3.26 log DNA copies/106 cells in LNs. Regression analysis shows that, in treated patients with sustained low viremia, cell-associated RNA and DNA in blood are better predictors of virus load in LNs than viremia.

Acquired Immunodeficiency Syndrome↗
PubMed2001

Human immunodeficiency virus Type 1 (HIV-1) plasma virus load and markers of immune activation among HIV-infected female sex workers with sexually transmitted diseases in Abidjan, Côte d'Ivoire.

Plasma levels of human immunodeficiency virus type 1 (HIV-1) RNA and markers of immune activation were compared among HIV-1-infected female sex workers (FSWs) with (n=112) and without (n=88) sexually transmitted diseases (STDs) in Abidjan, Côte d'Ivoire. After adjustment for CD4+ T cells, the median virus load was 2.5-fold higher among HIV-seropositive FSWs with STDs than among those without an STD (P=.053). Median virus load was higher for FSWs with a genital ulcer (P=.052) or gonorrhoea (P=.058) than for FSWs without any STD. Median levels of markers of immune activation (CD38 and HLA-DR on CD8+ T cells, soluble tumor necrosis factor-alpha receptor II, and beta(2)-microglobulin) tended to be elevated, albeit nonsignificantly, among FSWs in the STD group. These findings have important public health implications in elaborating strategies for decreasing disease progression and transmission of HIV among FSWs.

Adult↗
PubMed1997

Detection rate and intratumoral virus load of human herpesvirus-8 in immunodeficiency-related B-cell lymphoid malignancies.

Human herpesvirus-8 (HHV-8), associated with Kaposi's sarcoma, primary effusion lymphoma, and Castleman's disease, has been found in circulating B-cells and might have a causative role in B-cell malignancies associated with immunodeficiency syndromes. We determined the rate of detection and intratumoral virus load of HHV-8 by means of a semiquantitative approach in post-transplant lymphoproliferative diseases (PTLDs), AIDS-related non-Hodgkin's lymphomas (NHLs), including both Burkitt's lymphomas (BLs) and large cell lymphomas (LCLs), as well as in control groups consisting of follicular hyperplasias (FHs) and HIV-negative LCLs. HHV-8 sequences were detected at a similar rate in HIV-negative PTLDs (24%), HIV-negative LCLs (22%) and HIV-negative FHs (17%). The detection rate was significantly higher in HIV-positive BLs (73%), HIV-positive LCLs (67%), and HIV-positive FHs (65%) supporting the view of an epidemiological link between HHV-8 and HIV infections. The viral load was 10(2) genome copies per cell in the single case of primary effusion lymphoma included in the LCL group while it was 10(-3) copy per cell (median value; range: 10(-4)-10(-1)) in all the other HHV-8-positive samples. No significant difference of viral load was found according to HIV status. The virus loads of PTLDs and HIV-positive LCLs were significantly higher than those observed in HIV-positive BLs and FHs, suggesting, to some extent, that the degree of immunodeficiency may influence HHV-8 replication. However, with the exception of the single case of primary effusion lymphoma studied, the low intratumoral load of HHV-8 strongly argues against a direct causative agent of the virus in the occurrence of PTLDs and AIDS-related NHLs.

Case-Control Studies↗
PubMed2002

Cytomegalovirus (CMV) virus load kinetics to predict recurrent disease in solid-organ transplant patients with CMV disease.

Despite standard therapy, cytomegalovirus (CMV) disease recurs in a significant proportion of organ transplant recipients. The kinetics of CMV load in response to therapy may allow early prediction of recurrence. CMV loads were obtained at regular intervals after starting ganciclovir therapy in 52 transplant recipients with CMV disease. Virus load kinetics were analyzed using decay curves to assess viral dynamics, including half-life and time to viral clearance. Recurrent CMV disease occurred in 12 (23%) of 50 patients. The time period to viral clearance was longer among patients with recurrence of CMV disease (P=.002), and lack of clearance was also associated among patients with disease recurrence (P<.001). Viral kinetics followed a logarithmic decay curve expressed by the equation y=y(0)e(-ax). Virus load half-life was 8.8 days among patients with recurrence versus 3.17 days among patients without recurrence (P=.001). This was not explainable by detectable ganciclovir resistance. CMV load kinetics are useful for identifying, at a very early stage, patients who are more likely to have recurrence.

Antiviral Agents↗
PubMed2000

Monitoring the virus load can predict the emergence of drug-resistant hepatitis B virus strains in renal transplantation patients during lamivudine therapy.

The development of resistant hepatitis B virus (HBV) strains during lamivudine treatment has been described repeatedly. To investigate whether the development of such resistant HBV strains can be predicted in an early phase of therapy, the HBV loads of 11 renal transplantation patients were screened at 3-month intervals by a quantitative HBV polymerase chain reaction (PCR) assay. Lamivudine resistance was detected by sequence analysis. Five patients developed resistance to lamivudine in the 12-15-month follow-up period. In all of them, a virus load of 1x103 HBV DNA copies still was detectable after 3 months of therapy. This was statistically significantly different from those patients who did not develop lamivudine resistance within the observation period, all of whom had no HBV DNA detectable after 3 months of treatment (P=.0022). Thus, virus load testing by use of a sensitive PCR assay allows the early prediction of the emergence of lamivudine-resistant HBV strains.

Adult↗
PubMed1997

The impact of active herpes simplex virus infection on human immunodeficiency virus load.

The effect of a concurrent herpes simplex virus (HSV) infection on human immunodeficiency virus type 1 (HIV-1) load was evaluated. Sixteen subjects were identified with an active HSV infection and had pre-outbreak, acute-phase, and post-outbreak plasma (n = 16) and peripheral blood mononuclear cell (PBMC) (n = 8) samples for evaluation. All subjects were treated for an acute HSV outbreak with acyclovir for 10 days, followed by chronic prophylaxis. HIV-1 plasma RNA levels were determined by branched DNA, and intracellular HIV gag mRNA copy numbers were determined by quantitative reverse transcriptase-polymerase chain reaction ELISA. Plasma virus load increased a median of 3.4-fold during the acute outbreak (range, 0- to 10-fold; P = .002), while post-outbreak levels (30-45 days after the appearance of lesions) remained above pre-outbreak, baseline levels in some subjects. Intracellular HIV gag mRNA increased during the outbreak as well. Thus, an acute HSV episode can result in increased HIV transcription and plasma virus load.

AIDS-Related Opportunistic Infections↗
PubMed2001

High virus loads in naturally and experimentally SIVagm-infected African green monkeys.

A quantitative RT-PCR assay was developed for SIVagm and was used to measure the levels of viral RNA in the plasma of experimentally and naturally infected African green monkeys. The number of productively infected PBMCs and the number of cells carrying integrated provirus were also measured. Plasma virus loads in experimentally infected animals peaked at 2 weeks postinfection, ranging from 2.9 x 10(5) to 4.2 x 10(7) RNA copies/ml plasma. Set points of 2.1 x 10(3) to 2.8 x 10(6) RNA copies/ml plasma were maintained for one year. Similarly, the number of cells carrying integrated SIVagm provirus remained relatively stable in individual animals for one year with set points ranging from 73 to 810 proviral copies per 10(6) PBMC. However, the number of productively infected cells fluctuated considerably during this period. Virus loads in the 26 naturally infected AGMs ranged from 8.3 x 10(3) to 1.1 x 10(7) (mean 1.7 x 10(6)) RNA copies/ml plasma. These levels of viremia are similar to those seen in pathogenic systems (HIV-1, SIVmac), indicating that control of SIVagm replication is not the reason for the natural host's resistance to disease progression.

Animals↗
PubMed2002

Sensitive enzyme immunoassay for hepatitis B virus core-related antigens and their correlation to virus load.

A sensitive enzyme immunoassay (EIA) specific for hepatitis B virus core antigen (HBcAg) and hepatitis B e antigen (HBeAg) was developed. We designated the precore/core gene products as hepatitis B virus (HBV) core-related antigens (HBcrAg). In order to detect HBcrAg even in anti-HBc/e antibody-positive specimens, the specimens were pretreated in detergents. The antibodies are inactivated by this pretreatment and, simultaneously, the antigens are released and the epitopes are exposed. The assay demonstrated 71 to 112% recovery using HBcrAg-positive sera. We observed no interference from the tested anticoagulants or blood components. When the cutoff value was tentatively set at 10(3) U/ml, all healthy control (HBsAg/HBV-DNA negative; n = 108) and anti-HCV antibody-positive (n = 59) sera were identified as negative. The assay showed a detection limit of 4 x 10(2) U/ml using recombinant antigen. Detection limits were compared in four serially diluted HBV high-titer sera. The HBcrAg assay demonstrated higher sensitivity than HBV-DNA transcription-mediated amplification (TMA) or HBeAg radio immunoassay (RIA) in the dilution test. HBcrAg concentrations correlated well with HBV-DNA TMA (r = 0.91, n = 29) and in-house real-time detection-PCR (r = 0.93, n = 47) in hepatitis B patients. On HBeAg/anti-HBe antibody seroconversion panels, the HBcrAg concentration changed in accordance with HBV-DNA levels. HBcrAg concentration provides a reflection of HBV virus load equivalent to HBV-DNA level, and the assay therefore offers a simple method for monitoring hepatitis B patients.

Animals↗
PubMed2000

Virus load and sequence variation in simian retrovirus type 2 infection.

The natural history of type D simian retrovirus (SRV) infection is poorly characterized in terms of viral load, antibody status, and sequence variation. To investigate this, blood samples were taken from a small cohort of mostly asymptomatic cynomolgus macaques (Macaca fascicularis), naturally infected with SRV type 2 (SRV-2), some of which were followed over an 8-month period with blood taken every 2 months. Provirus and RNA virus loads were obtained, the samples were screened for presence of antibodies to SRV-2 and neutralizing antibody titers to SRV-2 were assayed. env sequences were aligned to determine intra- and intermonkey variation over time. Virus loads varied greatly among cohort individuals but, conversely, remained steady for each macaque over the 8-month period, regardless of their initial levels. No significant sequence variation was found within an individual over time. No clear picture emerged from these results, which indicate that the variables of SRV-2 infection are complex, differ from those for lentivirus infection, and are not distinctly related to disease outcome.

Animals↗
PubMed2004

Long-term efficacy and safety of protease inhibitor switching to nevirapine in HIV-infected patients with undetectable virus load.

BACKGROUND: Simplified highly active antiretroviral therapy (HAART) regimens are becoming widely used, particularly as a result of the side effects of and difficult compliance with protease inhibitor (PI) therapy. However, the long-term efficacy of HAART has not been properly assessed. METHODS: We performed a prospective study of 110 patients infected with human immunodeficiency virus type 1 (HIV-1) with undetectable virus load who discontinued PI therapy and initiated therapy with nevirapine without changing nucleoside analogues. Reasons for switching were treatment simplification (45%), lipodystrophy (24%), renal problems (23%), and dyslipidemia (8%). HIV-1 load, CD4 cell count, and fasting biochemistry profiles were performed at the time of switching (baseline) and every 3-4 months thereafter. The aim of the study was to evaluate the long-term efficacy and safety of this combination. RESULTS: Sixty-eight patients (61.8%) had a duration of follow-up of 3 years. The mean increase in the CD4 cell count after 3 years was 90 cells/microL (13.8% from baseline). Virus loads remained undetectable in all patients but 9 (8.2%). Triglyceride levels dramatically improved at 12 months (a 75% decrease; P<.02) and remained statistically significant over time (P<.04). The same occurred with serum cholesterol levels: there was an initial reduction of 25% (P<.02) and at the end of the follow-up period (P<.015). However, at the long-term evaluation, complete normalization of mean serum cholesterol and triglyceride levels could not be achieved. Sixteen patients (14.5%) had to stop therapy as a result of nevirapine-associated side effects. CONCLUSIONS: The switching of a PI to nevirapine is a safe and well-tolerated option for maintaining long-term virological suppression and immunological control. Three years after starting nevirapine therapy, rates of hypercholesterolemia and hypertriglyceridemia improved, although normal cholesterol and triglyceride values were not achieved.

Adult↗
PubMed2001

Macrophage are the principal reservoir and sustain high virus loads in rhesus macaques after the depletion of CD4+ T cells by a highly pathogenic simian immunodeficiency virus/HIV type 1 chimera (SHIV): Implications for HIV-1 infections of humans.

The highly pathogenic simian immunodeficiency virus/HIV type 1 (SHIV) chimeric virus SHIV(DH12R) induces a systemic depletion of CD4(+) T lymphocytes in rhesus monkeys during the initial 3-4 weeks of infection. Nonetheless, high levels of viral RNA production continue unabated for an additional 2-5 months. In situ hybridization and immunohistochemical analyses revealed that tissue macrophage in the lymph nodes, spleen, gastrointestinal tract, liver, and kidney sustain high plasma virus loads in the absence of CD4(+) T cells. Quantitative confocal immunofluorescence analysis indicated that greater than 95% of the virus-producing cells in these tissues are macrophage and less than 2% are T lymphocytes. Interestingly, the administration of a potent reverse transcriptase inhibitor blocked virus production during the early T cell phase but not during the later macrophage phase of the SHIV(DH12R) infection. When interpreted in the context of HIV-1 infections, these results implicate tissue macrophage as an important reservoir of virus in vivo. They become infected during the acute infection, gradually increase in number over time, and can be a major contributor to total body virus burden during the symptomatic phase of the human infection.

Adenine↗