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At least 649 records · Page 36Linked to original sources
PubMed2003

Dynamics of viral load rebound in plasma and semen after stopping effective antiretroviral therapy.

A rebound in the plasma and seminal viral load was detected in 12 patients after the interruption of effective highly active antiretroviral therapy. The viral rebound was generally higher in plasma, although the highest level observed during interruption was higher in semen in two patients. The reintroduction of therapy was followed by an overall decrease in HIV-RNA in plasma and semen. One to 2 months after restarting treatment, four out of seven patients showed undetectable HIV-RNA in semen.

Antiretroviral Therapy, Highly Active↗
PubMed1999

Short-term effects of large-dose vitamin A supplementation on viral load and immune response in HIV-infected women.

Vitamin A supplementation has been suggested for treatment and prevention of HIV infection. However, some in vitro data indicate that vitamin A may activate HIV. Randomly, 40 HIV-seropositive women of reproductive age were allocated to receive a single oral dose of 9900 micromol (300,000 IU) vitamin A or placebo. Plasma HIV-1 RNA concentration, total lymphocytes, selected lymphocyte subsets and activation markers, and in vitro lymphocyte proliferation to phytohemagglutinin (PHA) and Candida were measured before dosing and at various time points over an 8-week follow-up period. No differences were found between treatment groups in the frequency of signs or symptoms of acute vitamin A toxicity, nor were differences evident in any lymphocyte subset or activation marker at any time during follow-up. Mean and median viral load concentration at each time point and change in viral load from baseline to each follow-up point did not differ between treatment groups. No difference was measured between treatment groups in the proportion of women who responded to PHA or Candida. This study provides no evidence that high dose vitamin A supplementation of HIV-infected women is associated with significant clinical or immunologic adverse effects.

Adult↗
PubMed2000

AIDS myelopathy is not associated with elevated HIV viral load in cerebrospinal fluid.

The pathogenesis of AIDS-associated myelopathy is unknown. Elevated HIV-1 viral load in CSF has been associated with cognitive impairment. The authors investigated if a similar association exists in patients with myelopathy. The authors evaluated levels of HIV-1 RNA in the CSF of 16 individuals with AIDS myelopathy and in 16 nonmyelopathic HIV-infected control subjects. There was no correlation between levels of HIV-1 RNA and the presence or severity of myelopathy.

Acquired Immunodeficiency Syndrome↗
PubMed2006

Measles viral load may reflect SSPE disease progression.

Subacute sclerosing panencephalitis (SSPE) is a rare, slowly progressive neurological disorder caused by the persistent infection with measles virus (MV). Despite much research into SSPE, its pathology remains obscure. We examined autopsy tissues of eight SSPE patients by real time quantitative PCR, immunohistochemistry and immunoblotting to determine viral load. MV N, M and H gene RNA could be detected in the central nervous system (CNS) of all patients and in two non-CNS tissues of one patient. The viral burden between patients differed up to four-fold by quantitative PCR and corresponded with detection of MV protein. The level of both viral RNA and antigen in the brain may correlate with disease progression.

Adolescent↗
PubMedDate not supplied

Differential viral loads of human papillomavirus 16 and 58 infections in the spectrum of cervical carcinogenesis.

Human papillomavirus (HPV) load was reported to be related to the severity of cervical neoplasia but with controversy. The viral load-disease severity relationship was showed in HPV 16, but no study was made in HPV 58, the second most prevalent HPV in cervical cancer in East Asia. We studied cervical HPV loads in HPV 16- and HPV 58-infected cases of normal, low-grade squamous intraepithelial lesions (LSIL), high-grade squamous intraepithelial lesions (HSIL), and invasive cervical cancer (CC) by using quantitative polymerase chain reaction (Q-PCR) with type-specific primers in defined cell number. With the exception of HPV 16 infection in normal, viral loads varied greatly in each disease regardless of genotypes. The load of HPV 16 differed significantly among disease severities, with a dramatic increase from normal (1.14 +/- 2.25 copies/cell) to LSIL, HSIL, and CC (1599 +/- 2301, 7489 +/- 24,087 and 1878 +/- 2979 copies/cell, respectively) (P < 0.01). No significant difference was noted among different HPV 58 infections, with loads in normal, LSIL, HSIL, and CC of 503 +/- 641, 7951 +/- 27,557, 353 +/- 744, and 1139 +/- 2895 copies/cell, respectively. In comparison with HPV 16, HPV 58 subclinical infection confers a significant higher load (P < 0.01). Different HPV types behave differentially in the spectrum of cervical carcinogenesis. Unlike HPV 16, the infection load of HPV 58 does not correlate to the clinical severity. The wide variation of HPV loads among different HPV types and among squamous intraepithelial lesions and CC makes the viral load test unrealistic in differentiating different severities of cervical neoplasia.

Adult↗
PubMed1996

Viral load and immunophenotype of cells obtained from lymph nodes by fine needle aspiration as compared with peripheral blood cells in HIV-infected patients.

We wished to establish the feasibility of fine needle aspiration of lymph nodes as a noninvasive method for measuring subsets of immune cells and viral load in HIV-infected patients. Twenty-five patients (CD4+ T cell range 4-760/microl, median 362) were selected. Lymph node aspiration was attempted in 21 patients. Lymph node cells (LNC), ranging from 6 x 10(3) to 2 x 10(6) (median 6 x 10(5)) were obtained in 17 subjects, and compared with peripheral blood mononuclear cells (PBMC) obtained simultaneously. Immunophenotype could be determined by flow cytometry in 9 patients. Mean percent of CD4+ CD3+ T cells in LNC and PBMC and 23.2 and 14.6. Mean percent of CD8+ CD3+ T cells in LNC and PBMC was 23.1 and 45.0, respectively. Therefore, CD4+/CD8+ ratios were much higher in LNC (mean +/- SD: 1.06 +/- 0.31) than in PBMC (0.35 +/- 0.13). The amount of HIV DNA (11 patients) and RNA (8 patients) was determined in the plasma, LNC, and PBMC by competitive reverse transcriptase-polymerase chain reaction (RT-PCR). The number of copies of viral DNA/10(5) cells was higher in LNC than in PBMC (LNC/PBMC ratio ranger: 0.54-25, median 3.4). The number of copies of unspliced viral RNA/10(5) cells was much higher in LNC than in PBMC (LNC/PBMC ratio range 65-1,159, median 435). The plasma RNA copy number, a measure of circulating cell-free virus, was correlated with the RNA copy number in PBMC, but not in LNC. A RT-PCR system specific for spliced transcripts was also used to assess the level of transcripts independent of genomic RNA. This assay also detected more signal in LNC than in PBMC. The level of spliced transcripts in LNC and PBMC correlated with the amount of full-length RNA detected by competitive PCR. A semiquantitative coculture assay with lymphoblasts from healthy donors was used to assess the infectivity of LNC as compared with PBMC in 14 patients. The minimum number of LNC necessary to cause a positive coculture ranged from 10(3) to > 10(5) (median 10(4)); the corresponding number for PBMC ranged from 10(3) to > 10(6) (median 5 x 10(5)). In most patients selected for palpable lymph nodes, LNC could be obtained by fine needle aspiration, thus allowing noninvasive monitoring of viral burden in lymphoid tissue. The present study also suggests that both T-cell subsets and viral load differ in the blood and lymphoid tissue, which raises the question of whether the study of the lymphoid tissue would yield better prognostic markers of disease course.

Adult↗
PubMed1995

Vertical Transmission of HIV-1. Correlation with maternal viral load and plasma levels of CD4 binding site anti-gp120 antibodies.

Almost all childhood HIV-1 is now acquired through vertical transmission. Identifying factors that affect the rate of transmission may lead to the initiation of specific preventive strategies. In this study, antibody levels against different neutralizing epitopes on the envelope glycoprotein of HIV-1 (gp120) were measured in HIV-1-infected pregnant women that either transmitted HIV-1 to their infants (18 women) or did not (29 women). Differences in levels of antibodies directed against the monomeric gp120 molecule and against the V3 loop region of gp120 were not significantly different between the two groups studied. However, significant differences were observed in the levels of CD4 binding site antibodies, as determined by the ability of diluted maternal plasma to inhibit binding of the CD4 binding site monoclonal antibody F105 (mAb F105) to monomeric gp120. In addition, more nontransmitting mothers had low viral load as defined by having two or more negative HIV-1 viral cultures during pregnancy compared with transmitters. This pilot study suggests that in addition to higher viral load, low levels of CD4 binding site antibodies correlate with increased risk of HIV-1 vertical transmission. Passive immunotherapy with broadly neutralizing CD4 binding site antibodies should be considered as a strategy to reduce this risk.

Acquired Immunodeficiency Syndrome↗
PubMed2003

Analysis of HIV-1 viral load in seminal plasma samples.

BACKGROUND: With HIV-1-infected individuals now facing the prospect of relatively long and healthy lives, many discordant couples (where the male is HIV-1 seropositive) are seeking to have children. To assist reducing the risks of heterosexual and subsequent vertical transmission in this situation, quantification of HIV-1 viral load in seminal plasma may be effective as one of several measures to reduce the risk of infecting the mother during insemination, potentially providing a better indication of infectivity than blood plasma analysis. OBJECTIVE(S): To modify existing molecular methods for the purpose of analysing HIV-1 viral load in seminal plasma. METHODS: Two commercial assays for HIV-1 RNA quantification were used to assess their sensitivity, specificity and precision for quantification of seminal plasma samples. Seminal plasma samples were prepared with an additional centrifugation step to aid removal of inhibitors to molecular assays. RESULTS: Seminal plasma samples exhibited specificity of >95%, equivalent to that reported by the manufacturers of the commercial assays. With additional centrifugation, complete inhibition of 2/19 (10%) seminal plasma samples was observed using the RT-PCR assay, and inhibition was not apparent in the bDNA assay. Quantification of HIV-1 RNA in seminal plasma samples in both assays was equivalent to that observed in plasma samples and did not appear to be affected by the additional centrifugation step. CONCLUSION: Minor modification of the RT-PCR assay procedure by additional centrifugation of seminal plasma improved the sensitivity of the assay. Inhibition was not apparent with the bDNA assay.

Female↗
PubMed2005

Quantitative EBV viral loads and immunosuppression alterations can decrease PTLD incidence in pediatric liver transplant recipients.

Epstein-Barr virus (EBV) is a common viral infection in pediatric liver transplant patients and can lead to development of post-transplant lymphoproliferative disorder (PTLD). Differing studies have used immunosuppression reduction, antiviral medications or i.v. CMV-immunogloublin for EBV prevention and treatment. The purpose of this study was to determine whether implementation of a protocol for frequent EBV monitoring and EBV viral load-driven immunosuppression reduction could decrease the incidence of PTLD in our patient population. All data were prospectively collected between 2001 and 2004 at a single institution. Seventy-three patients were entered into the study. Patients were divided into a historical control group (pre-2001, 30 patients) and a treatment group (post-2001, 43 patients). Approximately 1271 blood samples of 73 patients were collected between 2001 and 2004. Eleven out of 43 patients received immunosuppression tapering due to high EBV viral loads (>4000 copies/microg DNA). One patient developed allograft rejection after immunosuppression modulation. Prior to 2001, the incidence of PTLD at our institution was 16%. After instituting a protocol for EBV monitoring, the incidence of PTLD decreased to 2% (p-value<0.05). These findings illustrate that frequent EBV viral load monitoring and preemptive immunosuppression modulation have an integral role in preventing PTLD in the pediatric liver transplant population.

Adolescent↗
PubMed2000

Adherence to protease inhibitors, HIV-1 viral load, and development of drug resistance in an indigent population.

OBJECTIVE: To examine the relationship between adherence, viral suppression and antiretroviral resistance in HIV-infected homeless and marginally housed people on protease inhibitor (PI) therapy. DESIGN AND SETTING: A cross-sectional analysis of subjects in an observational prospective cohort systematically sampled from free meal lines, homeless shelters and low-income, single-room occupancy (SRO) hotels. PARTICIPANTS: Thirty-four HIV-infected people with a median of 12 months of PI therapy. MAIN OUTCOMES: Adherence measured by periodic unannounced pill counts, electronic medication monitoring, and self-report; HIV RNA viral load; and HIV-1 genotypic changes associated with drug resistance. RESULTS: Median adherence was 89, 73, and 67% by self-report, pill count, and electronic medication monitor, respectively. Thirty-eight per cent of the population had over 90% adherence by pill count. Depending on the measure, adherence explained 36-65% of the variation in concurrent HIV RNA levels. The three adherence measures were closely related. Of 20 genotyped patients who received a new reverse transcriptase inhibitor (RTI) when starting a PI, three had primary protease gene substitutions. Of 12 genotyped patients who received a PI without a new RTI, six had primary protease gene substitutions (P < 0.03). CONCLUSION: A substantial proportion of homeless and marginally housed individuals had good adherence to PI therapy. A strong relationship was found between independent methods of measuring adherence and concurrent viral suppression. PI resistance was more closely related to the failure to change RTI when starting a PI than to the level of adherence.

Adult↗
PubMed1998

[Quantitation of viral load in patients infected with HIV-1 subtype E or A].

Quantitation of viral load in a HIV infected person gives important information for monitoring of the clinical status of the patients and evaluation of anti viral effects of admininstred drugs. Although conventional Amplicor HIV-1 monitor system (Roche's conventional method) is used widely, the sensitivity of this system is not enough for measurement of subtype E and A giving lower titer of these subtype viruses than the actual quantity. In Japan, HIV-1 subytpe B cases used to be predominant but recently subtype E cases are increasing especially among heterosexuals thus it becomes required to increase the sensitivity of measurement of HIV-1 RNA of subtype E or A. Therefore we establised the Kanagawa primer method using newly developed subtype E and A primers added to the primers of Roche's conventional method. The results were compared with the conventional Amplicor and also with Roche's new version method which contained new primers. Kanagawa primer method gave 4 to 16 times more sensitive results as compared with Roche's conventional method for subtype E measurement. As for subtype A case, Kanagawa primer method gave a value 1.2 x 10(4) copies/ml while it was undetectable by Roche's conventional method. Roche's new version method showed equal sensitivity of Kanagawa primer method. As for subtype B, the results of these three methods showed no difference. Addition of our newly developed subtype E and A primers to the Roche's conventional method enabled to measure subtype E and A with high sensitivity. For quantitative measurement of HIV-1 RNA, it is important to consider the subtype of the virus in test samples.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Concentrations of circulating beta-chemokines do not correlate with viral load in human immunodeficiency virus-infected individuals.

The CC or beta-chemokines MIP-1alpha, MIP-1beta, and RANTES are the primary components of human immunodeficiency virus type 1 (HIV-1)-suppressive soluble factors in vitro. We studied the relationship between the concentrations of MIP-1alpha, MIP-1beta, and RANTES in plasma and HIV viral load in HIV-infected subjects. The HIV-positive patient group (n = 140) had significantly lower concentrations of all three beta-chemokines (MIP-1alpha, P < 0.0005; MIP-1beta, P < 0.005; RANTES, P < 0.0005) than the control group (n = 58 for MIP-1alpha, n = 27 for MIP-1beta, and n = 59 for RANTES). In addition, we divided the patient group into three subgroups (high, moderate, and low) based on the number of HIV-1 RNA copies in the plasma (as measured by quantitative HIV RNA PCR). Again, all three subgroups had significantly lower concentrations of the beta-chemokines than the HIV-negative control group. However, there was no significant difference in plasma beta-chemokine concentrations among the three subgroups within the patient group (P < 0.3). Although our results demonstrate that HIV-infected individuals had significantly lower concentrations of circulating beta-chemokines than healthy uninfected control subjects, we found no correlation between the concentrations of beta-chemokines in plasma and HIV-1 viral load in HIV-infected individuals.

CD4-Positive T-Lymphocytes↗
PubMed1999

Patients failing saquinavir therapy require an early change to indinavir before HIV-1 viral load reaches high levels.

Sequential use of antiretroviral therapy with protease inhibitors (PI) is frequently prescribed owing to failure or intolerance of the first selected agent. Controversial data exist about the virological and immunological outcome of patients in whom a change to a second PI regimen is needed. A prospective study of 113 HIV-positive patients (male, 84%; mean age 36 years; previous AIDS-defining event, 35%; previous antiretroviral therapy with nucleoside analogues, 94%) who started a saquinavir-containing regimen between March 1996 and March 1997 and had to change to indinavir (n = 79) owing to intolerance, failure or medical criteria was performed. At the time of the switch, median CD4 cell count was 221 cells/mm3 and the HIV RNA level was 3.98 log10 copies/ml. The rate of viral suppression (HIV RNA levels below 200 copies/ml) was 40% at 3 months and 28% at month 6 after indinavir was instituted. In a logistic regression analysis, only the baseline viral load [relative risk (RR), 2.85; 95% confidence interval (CI), 1.31-6.05; P = 0.007] was statistically associated with the lack of viral suppression on indinavir. Although there are not sufficient data about the best therapeutic option if a change in PI-containing regimens therapy is considered, this study supports the recommendation of an early change of the PI-containing regimens, before the HIV-1 viral load reaches high levels.

Acquired Immunodeficiency Syndrome↗
PubMed2002

HIV-1 RNA viral load monitoring in HIV-infected drug users on antiretroviral therapy: relationship with outpatient care patterns.

HIV-1 viral load (VL) testing is a standard component of HIV care. We examined the use and predictors of VL testing in drug users, a group at risk for problematic care. Using 1996 to 1998 New York State (NYS) Medicaid files, we studied drug users who had been enrolled >10 months, had been prescribed antiretroviral agents in 1997 and 1998, and who had undergone any VL testing in 1997. Our outcome was regular VL testing shown by two or more paid claims for this test in 1998. Patterns of care in 1997 were defined as: regular source of medical care (>35% of visits to one provider), and/or regular drug treatment of >6 months, or neither. We counted visits in 1997 to a provider offering HIV-focused care. Adjusted odds ratios (AORs) of VL testing were assessed. Of 3131 drug users, 73.9% had at least one VL test, whereas 56.2% had two or more VL tests in 1998. The AORs of two or more VL tests were increased for those with regular drug abuse care alone (AOR, 1.50; 95% confidence interval [CI], 1.21-1.84) or with regular medical care (AOR, 1.27; 95% CI, 1.03-1.57) versus those with neither. HIV-focused care was positively associated with two or more VL tests (AOR, 1.38; 95% CI, 1.05-1.81 for 1-3 visits; AOR, 1.94; 95% CI, 1.50-2.51 for four or more visits). We found that nearly half this cohort of drug users did not have regular VL testing. Drug users with HIV-focused care or with regular drug treatment are more likely to have regular VL testing.

Adult↗
PubMed1996

The effect of high-dose saquinavir on viral load and CD4+ T-cell counts in HIV-infected patients.

OBJECTIVE: To evaluate the efficacy and safety of high-dose therapy with the human immunodeficiency virus (HIV) protease inhibitor saquinavir and to establish the duration of the effect of this therapy. DESIGN: Open-label study. SETTING: Clinical research referral center. PATIENTS: 40 adults with human immunodeficiency virus type 1 (HIV-1) infection and CD4+ T-cell counts of 200 to 500 cells/mm3. INTERVENTION: Monotherapy with 3600 mg or 7200 mg of saquinavir per day, in six divided doses, for 24 weeks. MEASUREMENTS: Patients were monitored for adverse events and were evaluated monthly for CD4+ T-cell count, HIV-1 viral load (as measured by reverse transcriptase polymerase chain reaction [PCR] for plasma HIV RNA levels), immune-complex-disassociated p24 antigen levels, peripheral blood mononuclear cell viral DNA levels (as measured by PCR), and resistance mutations to saquinavir. Quantitative peripheral blood mononuclear cell cultures were also done every 2 months. RESULTS: The low-dose saquinavir regimen (3600 mg/d) resulted in a maximal mean decrease in plasma HIV RNA levels of 1.06 log RNA copies/mL of plasma and a mean maximal increase in CD4 counts of 72 cells/mm3. At week 24, the plasma HIV RNA level remained 0.48 log RNA copies/mL of plasma lower than baseline (P < 0.001) and the CD4 count remained 31 cells/mm3 higher than baseline (P = 0.165). The high-dose saquinavir regimen (7200 mg/d) produced a mean maximal decrease in the plasma HIV RNA level of 1.34 log RNA copies/mL of plasma and a mean maximal increase in CD4 count of 121 cells/mm3. At week 24, the plasma HIV RNA level remained 0.85 log RNA copies/mL of plasma lower than baseline (P < 0.001) and the CD4 count remained 82 cells/mm3 higher than baseline (P = 0.002). The high-dose regimen produced a greater reduction in plasma HIV RNA level (P = 0.08), a greater reduction in peripheral blood mononuclear cell cultures (P = 0.008), and a greater increase in CD4 count (P = 0.002) than did the low-dose regimen. Higher plasma drug concentrations in individual patients correlated with greater reductions in plasma HIV RNA levels over the two doses. Nine patients receiving the low-dose regimen and four patients receiving the high-dose regimen developed key saquinavir resistance mutations. Adverse reactions, most commonly gastrointestinal problems and elevated serum aminotransferase levels, were more common in patients receiving the high-dose regimen, but most adverse events were mild and all were reversible. CONCLUSION: Saquinavir is a potent antiviral agent that has a favorable toxicity profile at high doses. Higher doses produce a greater and more durable suppression of viral load and elevation in CD4+ T-cell counts and may delay the development of resistance mutations. Therapy with high-dose saquinavir alone or in combination with other antiretroviral agents should be investigated further.

Adult↗
PubMed2004

Mother-to-child transmission of HIV-1: strong association with certain maternal HLA-B alleles independent of viral load implicates innate immune mechanisms.

The transmission of HIV-1 from mother to child during pregnancy is unlike other types of HIV-1 transmission because the child shares major histocompatibility complex (MHC) genes with the mother during a time while the mother is induced to tolerate the paternally derived fetal MHC molecules, in part through natural killer (NK) recognition of MHC polymorphisms. The relevance of these immune mechanisms to HIV-1 transmission was assessed by determining the HLA-B alleles of mother and infant. Almost half (48%) of mothers who transmitted with low viral loads had HLA-B*1302, B*3501, B*3503, B*4402, or B*5001 alleles, compared with 8% of nontransmitting mothers (P=0.001). Conversely, 25% of mothers who did not transmit despite high viral loads had B*4901 and B*5301, vs. 5% of transmitting mothers (P=0.003), a pattern of allelic involvement distinct from that influencing HIV-1 infection outcome. The infant's HLA-B alleles did not appear associated with transmission risk. The HLA-B*4901 and B*5301 alleles that were protective in the mother both differed respectively from the otherwise identical susceptibility alleles, B*5001 and B*3501, by 5 amino acids encoding the ligand for the KIR3DL1 NK receptor. These results suggest that the probable molecular basis of the observed association involves definition of the maternal NK recognition repertoire by engagement of NK receptors with polymorphic ligands encoded by maternal HLA-B alleles, and that the placenta is the likely site of the effect that appears to protect against transmission of maternal HIV-1 through interrelating adaptive and innate immune recognition.

Adolescent↗
PubMed1999

Viral load and neuropathology in the SIV model.

To investigate neuropathological processes involved in HIV infection, a longitudinal analysis of central nervous system (CNS) changes was performed using the SIV-infected macaque model. Five animals were studied during the early phase and 13 during the asymptomatic and symptomatic phases. Histopathological analyses were performed on one cerebral fixed hemisphere whereas on the other frozen hemisphere in situ hybridisation, immunohistochemistry and RT-PCR were performed. Viral load was quantified by in situ hybridisation, CD4 and CD8 T cell infiltration by immunohistochemistry and mRNA cytokine expression (IL1beta, IL2, IL6, TNFalpha, IFNgamma and TGF-beta1) by semiquantitative RT-PCR. As reported for HIV-infected humans, the neuropathological analysis of SIV infected animals revealed four distinct lesion profiles: minimal changes, early encephalitis, leukoencephalopathy and encephalitis. No relationship was found between neuropathological findings, numbers of SIV replicating cells and T cell infiltration. CNS infection was found to be an early event characterised by glial activation, an increase in the level of IL1beta, TNFalpha and IL6 mRNA expression. During the asymptomatic and symptomatic phases, IL6 and IL1beta mRNAs increase coincided with gliosis and the development of myelin lesions. The absence of relationship between neuropathological findings and viral load suggests that cerebral lesions are caused by an indirect mechanism. Inflammatory cytokine pattern associated with severe lesions show the key role of glial activation in the SIV neuropathological process.

AIDS Dementia Complex↗