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PubMed1999

Long-term stability of human immunodeficiency virus viral load and infectivity in whole blood.

BACKGROUND: We intended to evaluate the stability of human immunodeficiency virus (HIV) type 1 virions in whole blood and in culture medium. MATERIALS AND METHOD: EDTA whole-blood samples taken from 12 patients were left at room temperature for up to 7 days, and aliquots of a laboratory virus stock spiked in EDTA, in heparinized or in citrated whole blood, with or without the addition of Triton X-100, or spiked in culture medium were left at room temperature for up to 120 days before plasma was separated and frozen at -80 degrees C. Viral load was measured for all frozen plasma samples using different viral load assays. p24 antigen and infectivity were also measured in the spiked samples. RESULTS: The patient whole-blood samples did not show any decrease in viral load during this 7-day period. The spiked samples decayed by not more than 1 log after 120 days (about 4 months), with the fastest decay in medium. Virus infectivity decayed very slowly from 20,000 units mL-1 to undetectable amounts after 56 days. CONCLUSIONS: These results indicate that HIV-1 virions in whole blood possess a long-term stability in terms of viral load, p24 antigen level and infectivity, which is not sufficiently recognized by laboratory and health care workers.

Freezing↗

PubMed2003

Successful HCV genotyping of previously failed and low viral load specimens using an HCV RNA qualitative assay based on transcription-mediated amplification in conjunction with the line probe assay.

BACKGROUND: Hepatitis C virus (HCV) genotyping is a critical part of the diagnostic work-up for chronic hepatitis C. The VERSANT HCV line probe assay (LiPA) marketed by Bayer Corporation requires PCR-derived amplicons for genotyping usually obtained from commercial assays, including Amplicor HCV 2.0 (Amplicor 2.0), Amplicor HCV Monitor 2.0, or SuperQuant. Occasionally, PCR-based methods in conjunction with LiPA fail to give a genotyping result. Although most genotyping failures occur among low viral load specimens, some occur in specimens with relatively high viral loads. The Bayer HCV RNA Qualitative assay (HCV TMA), with a limit of detection of approximately 5-10 IU/ml, is more sensitive than other commercial assays. OBJECTIVES: An HCV genotyping protocol using HCV TMA linked with LiPA (TMA-LiPA) was developed and tested for ability to genotype samples that had previously failed genotyping by PCR-based methods in conjunction with LiPA. STUDY DESIGN: Clinical specimens were obtained from eight independent laboratories in Canada and the US and tested with TMA-LiPA at the Bayer Reference Testing Laboratory. Specimens included those that failed to produce a genotype result when a PCR-based assay was used in conjunction with LiPA and specimens for which genotyping was not attempted because the viral load was below the validated cut-off determined in the laboratory of origin. RESULTS AND CONCLUSIONS: TMA-LiPA successfully genotyped 68 of 75 (90.7%) specimens that had failed genotyping by PCR-based methods used in conjunction with LiPA and 36 of 40 (90.0%) specimens that were rejected for genotyping due to low viral load. Moreover, TMA-LiPA assigned subtype for 79 of 107 (73.8%) specimens. Our TMA-LiPA results reflected the distribution of HCV genotypes found in North America, and were 100% concordant with those of Amplicor 2.0 in conjunction with LiPA for control specimens genotyped by both assays. TMA-LiPA may prove useful both in optimizing LiPA performance and genotyping patient specimens.

Genotype↗

PubMed2003

Polyomavirus allograft nephropathy: sequential assessment of histologic viral load, tubulitis, and graft function following changes in immunosuppression.

Our initial cases of polyoma virus allograft nephropathy (PVAN) received pulse steroids due to anxiety about concomitant acute rejection triggered by the presence of tubulitis. However, our current policy is to reduce immunosuppression in all cases. The aim of this study was to determine whether clinical follow-up in these patient categories shows any differences in: (a) histologic viral load, (b) grade of tubulitis, and (c) graft function. Reduced viral load assessed within 8 weeks was seen in 4/20 (20.0%) biopsies treated initially by increased immunosuppression, compared to 15/19 (83.3%) biopsies treated with reduced immunosuppression (p = 0.001, Fisher's exact test). Yet, >70% reversal of the rise in serum creatinine occurred in only 3/19 (15.8%) and 1/19 (5.3%) patients, respectively, in these two groups. Improved tubulitis was seen in 11/20 (55%) of biopsies treated with steroids, despite the lack of beneficial effect on serum creatinine in 12/19 (63.1%) instances. In biopsies not treated with any change in immunosuppression, the serum creatinine remained stable in 1/5 (20%) and worsened in 4/5 (80%) biopsies. These data demonstrate that in biopsies with PVAN and tubulitis, reduced immunosuppression is more effective in lowering viral load than steroid therapy. Lack of parallelism between viral load, tubulitis grade, and serum creatinine illustrates a complex interplay of viral and alloimmune factors leading to graft injury.

Adult↗

PubMed1999

Significance of qualitative polymerase chain reaction combined with quantitation of viral load in the diagnosis and follow-up of cytomegalovirus infection after solid-organ transplantation.

Quantitative PCR was evaluated in the monitoring of patients with ongoing posttransplantation cytomegalovirus (CMV) infection and antiviral therapy, compared to leukoDNAemia and serology. From January 1998 until May 1999, 61 patients were followed up weekly during 3 months after transplantation by a qualitative PCR. The quantitative PCR was performed on plasma samples from 21 selected patients, of whom 12 had a primary infection and 9 a reactivation or reinfection. Analysis of the viral load differences showed that the viral loads in patients with a primary infection were significantly higher than viral loads in patients with a reactivation (p < 0.01). Based on the results of our study, we can state that qualitative PCR is a good marker for initiating preemptive therapy. In addition, viral quantitation is clinically useful for accurate diagnosis of established CMV disease, and monitoring of antiviral therapy.

Antiviral Agents↗

PubMed1998

Rate of HIV-1 decline following antiretroviral therapy is related to viral load at baseline and drug regimen.

OBJECTIVES AND DESIGN: The dynamics uf viral decline following the initiation of antiretroviral treatment were studied in 29 HIV-1-infected patients participating in a two-arm trial comparing immediate (group A: ritonavir, zidovudine and lamivudine) and delayed (group B: ritonavir supplemented by zidovudine and lamivudine on day 21) triple therapy. Parameters underlying viral dynamics were estimated using mathematical models tailored to these treatment protocols. RESULTS: The decline in plasma HIV-1 density between day 0 and 21 was steeper in group A (-2.27+/- 0.46 log10) than group B (-1.87+/-0.56 log10). In a subset of patients amenable to full mathematical analysis, a short-lived productively infected cell compartment (producing approximately 97% of total virions) decayed with a half-life of 1.0-2.5 days, whereas a long-lived infected cell compartment decayed with a half-life of 18.8-32.8 days. Estimates for the time for the elimination of virus from these two cell populations ranged from 474 to 802 days. The rate of loss of productively infected CD4+ T cells was positively correlated with baseline viral load in group A and in the combined dataset. CONCLUSIONS: These results suggest that HIV-infected cell populations may have a faster turnover in patients with higher viral loads due to higher infection rate parameters, higher rates of virus production, or lower virus clearance rates.

Anti-HIV Agents↗

PubMed1998

Predictive value of viral load and other markers for progression to clinical AIDS after CD4+ cell count falls below 200/microL. SEROCO & HEMOCO Study Group.

BACKGROUND: To assess the predictive value of biological and clinical events for progression to AIDS (1993 European classification) when the CD4+ cell count falls below 200/microL (CD4 threshold) in different exposure groups. To investigate whether such markers remain predictive independently of the serum HIV-1 RNA level at the CD4 threshold. METHODS: The predictive value of biological and clinical events occurring during the 24 months prior to the occurrence of CD4 threshold (n = 333) was quantified in a Cox model. Another Cox model was carried out in a subset of 77 patients in whom viral load from stored sera was available. Furthermore, changes in viral load during the 24 months preceding the CD4 threshold were assessed in a mixed model according to subsequent development of AIDS. RESULTS: Among the 333 patients, the slope of the CD4+ cell counts, the emergence of p24 antigen, persistent thrush, and age at the CD4 threshold were independent predictors of progression to clinical AIDS (44.7%). Among the subset of 77 patients, the HIV-1 RNA level at the CD4 threshold, persistent thrush and age remained independent predictors of progression to AIDS (45.5%). The increase of the HIV-1 RNA level was moderate, both in non-progressors (24.0% per year) and in those who subsequently developed AIDS (27.1% per year), (P = 0.93). Viral load was consistently higher in the latter group (P = 0.002). CONCLUSION: At a late stage of infection, age and persistent thrush remain predictive of progression to AIDS, independently of viral load.

Acquired Immunodeficiency Syndrome↗

PubMed2004

High viral loads despite absence of clinical and pathological findings in cats experimentally infected with feline coronavirus (FCoV) type I and in naturally FCoV-infected cats.

Specified pathogen-free cats were naturally infected with FCoV or experimentally infected with FCoV type I. Seroconversion was determined and the course of infection was monitored by measuring the FCoV loads in faeces, whole blood, plasma and/or monocytes. Tissue samples collected at necropsy were examined for viral load and histopathological changes. Experimentally infected animals started shedding virus as soon as 2 days after infection. They generally displayed the highest viral loads in colon, ileum and mesenteric lymph nodes. Seroconversion occurred 3-4 weeks post infection. Naturally infected cats were positive for FCoV antibodies and monocyte-associated FCoV viraemia prior to death. At necropsy, most animals tested positive for viral shedding and FCoV RNA was found in spleen, mesenteric lymph nodes and bone marrow. Both experimentally and naturally infected cats remained clinically healthy. Pathological findings were restricted to generalized lymphatic hyperplasia. These findings demonstrate the presence of systemic FCoV infection with high viral loads in the absence of clinical and pathological signs.

Animals↗

PubMedDate not supplied

[The relationship between viral load and malondialdehyde and antioxidant enzymes in patients with hepatitis C virus infection].

Oxidative stress is known to participate in the pathogenesis of HCV infection. The aim of this study was to investigate the relationship between antioxidant defence state, malondialdehyde (MDA) and viral load in patients with hepatitis C virus (HCV) infection. Fifty patients who were positive for serological and molecular markers of HCV infection, and 40 healthy volunteers as control group were included in the study. The patients were classified according to their viral loads, and the catalase, superoxide dismutase (SOD) and glutathione peroxidase (GP) activities of erythrocytes and MDA in sera of all groups were measured. These substances were detected by using the methods described by Aebi, Woolliams et al, Paglia and Valentine, Draper and Hadley, respectively. As a result, decrease in SOD and GP levels and increase in MDA and catalase levels have been detected in HCV infected patients when compared with healthy controls, and these differences were statistically significant (p<0.05, t=19.3),except for catalase. However, there were no statistically significant difference among groups classified according to viral load (p>0.05, t=1.6). Although our data in HCV infected patients demonstrate a significant decrease in antioxidant enzyme levels and a significant increase in MDA levels, a marker of oxidative stress, it could not possible to make a correlation between these differences and the viral loads of patients.

Case-Control Studies↗

PubMed1998

HIV-1-infected long-term slow progressors heterozygous for delta32-CCR5 show significantly lower plasma viral load than wild-type slow progressors.

OBJECTIVE: Patients heterozygous for delta32-CCR5 may have a delayed progression of HIV-1 disease. The aim of the present study was to investigate the influence of CCR5/delta32-CCR5 genotype in long-term slow progressors using plasma viral load as a marker of disease progression. DESIGN: We analyzed 70 long-term slow progressors (diagnosis > 8 years previously; CD4 count > 500/microl; asymptomatic, never received antiretroviral therapy) for CCR5 genotype, plasma viral load, and lymphocyte subsets. Distribution of CCR5 genotypes was compared with a cohort of 61 multiply exposed noninfected individuals and a group of 336 control subjects. All study participants were white. METHODS: CCR5 genotype was determined by polymerase chain reaction (PCR) amplification. Plasma viral load was quantified by branch DNA hybridization, lymphocyte subsets were determined by fluorescence-activated cell sorter (FACS) analysis. The Mann-Whitney-Wilcoxon test was used for statistical analyses. RESULTS: The frequency of the CCR5/delta32-CCR5 heterozygote genotype was higher in long-term slow progressors (37.1%) and multiply exposed noninfected individuals (26.2%), compared with the control group (15.8%). In addition, plasma viral load was found to be significantly lower in CCR5/delta32-CCR5 heterozygous long-term slow progressors (median < log10 2.70; 53.8% < log10 2.70; 0% > log10 4.0) relative to that seen in CCR5/CCR5 long-term slow progressors (median log10 3.64; 22.7% < log10 2.70; 22.7% > log10 4.0). CONCLUSIONS: These findings strengthen the hypothesis of a favorable influence of CCR5/delta32-CCR5 genotype on progression of HIV-1 infection. Therefore, evaluation of CCR5 genotype might influence antiretroviral therapy strategies in early stages of HIV-1 infection.

Cohort Studies↗

PubMed1996

Hepatitis C plasma viral load is associated with HCV genotype but not with HIV coinfection.

The influence of human immunodeficiency virus (HIV) coinfection and hepatitis C virus (HCV) genotype distribution on HCV viral load and alanine amino transferase (ALT) levels in chronically infected patients remains unclear. In the present study, serum samples from a group of haemophiliac patients were investigated retrospectively. HCV geno- and subtyping was carried out using the Inno line probe assay (Inno LIPA, Innogenetics, Zwijnaarde, Belgium) in 87 patients positive by HCV RT PCR. Of these patients, 31 (35.6%) were HIV coinfected. HCV RNA was quantified with the HCV Monitor kit (Roche, Basel, Switzerland) in 43 patients (22 HIV-negatives, 21 HIV-positives). The most prevalent genotypes were 1 (n = 52) and 3a (n = 16) followed by genotype 2 (n = 9) and 4 (n = 3). Mixed infections were detected in 7 patients. Of genotype 1 positive samples, 24 and 23 were classified as subtype a and b, respectively. Five samples could not be subtyped. Although higher mean values of ALT were observed in genotype 1 infected patients, there was no statistically significant association between HCV genotype or subtype and liver enzymes (P > 0.05). On the other hand, statistically significant higher HCV RNA titres were observed in haemophiliacs infected with HCV genotype 1 in comparison to those infected with other genotypes (P < 0.01). No relationship was found between the presence of HIV coinfection and viral load of HCV RNA. There was no evidence that HCV infection had a more severe outcome in HIV-positive patients who had been infected with HIV and HCV more than ten years ago, even in those with very low CD4+ cell counts. No clear association between high ALT levels and large amounts of viral RNA was observed. In conclusion, a large viral load is associated with HCV genotype 1 infection; HIV coinfection has no clear effect on the intensity of HCV replication. An ongoing prospective study will evaluate the respective role of viral load, genotype, HIV coinfection and ALT level in the response to interferon therapy.

Alanine Transaminase↗

PubMed1998

Heterosexual HIV-1 transmission and viral load in hemophilic patients.

Only one fifth or fewer of the female sexual partners of HIV-1-infected men with hemophilia become infected. The risk factors associated with heterosexual transmission of HIV-1 are not well understood. To investigate the hypothesis that HIV-1 viral load may be related to heterosexual HIV-1 transmission, we measured HIV-1 RNA by polymerase chain reaction (PCR) in frozen samples from 39 men with hemophilia and HIV-1 infection obtained between 20 and 62 months after HIV-1 seroconversion, during at least a 6-month relationship with a female sexual partner. The median time from the hemophilic viral load determination to the estimated date of transmission to the female partner was 9 months (range, 4-41 months). The proportion of HIV-positive hemophilic men with >100,000 HIV RNA copies/ml was significantly higher in transmitters (TR) (3 of 5 [60%]), than in nontransmitters (NTR) (3 of 34 [9%]; p = 0.027). There were no differences between TR and NTR in age at seroconversion (32.4 years each), in time from seroconversion to AIDS (67 versus 79 months), in mean CD4 number (245/microl] versus 260/microl); nor in the proportion who developed AIDS (4 of 5 [80%] versus 24 of 34 [71%]). These findings appear to suggest that high HIV viral load in HIV-infected hemophilic men increases the risk of HIV transmission to heterosexual partners. Viral load determinations may be helpful in counseling hemophilic couples regarding transmission to female partners.

Disease Transmission, Infectious↗

PubMed1999

High viral load in the cerebrospinal fluid and brain correlates with severity of simian immunodeficiency virus encephalitis.

AIDS dementia and encephalitis are complications of AIDS occurring most frequently in patients who are immunosuppressed. The simian immunodeficiency virus (SIV) model used in this study was designed to reproducibly induce AIDS in macaques in order to examine the effects of a neurovirulent virus in this context. Pigtailed macaques (Macaca nemestrina) were coinoculated with an immunosuppressive virus (SIV/DeltaB670) and a neurovirulent molecularly cloned virus (SIV/17E-Fr), and more than 90% of the animals developed moderate to severe encephalitis within 6 months of inoculation. Viral load in plasma and cerebrospinal fluid (CSF) was examined longitudinally to onset of AIDS, and viral load was measured in brain tissue at necropsy to examine the relationship of systemic and central nervous system (CNS) viral replication to the development of encephalitis. In all animals, plasma viral load peaked at 10 to 14 days postinfection and remained high throughout infection with no correlation found between plasma viremia and SIV encephalitis. In contrast, persistent high levels of CSF viral RNA after the acute phase of infection correlated with the development of encephalitis. Although high levels of viral RNA were found in the CSF of all macaques (six of six) during the acute phase, this high level was maintained only in macaques developing SIV encephalitis (five of six). Furthermore, the level of both viral RNA and antigen in the brain correlated with the severity of the CNS lesions. The single animal in this group that did not have CNS lesions had no detectable viral RNA in any of the regions of the brain. The results substantiate the use of CSF viral load measurements in the postacute phase of SIV infection as a marker for encephalitis and CNS viral replication.

Animals↗

PubMed1997

Maternal HIV-1 viral load and vertical transmission of infection: the Ariel Project for the prevention of HIV transmission from mother to infant.

Most HIV-1 infections of children result from mother-to-infant transmission, which may occur perinatally or postnatally, as a consequence of breast feeding. In this study, the influence of maternal viral load on transmission of infection to infants from non-breast-feeding mothers was examined using samples of plasma and peripheral blood mononuclear cells (PBMCs) collected at several time points during pregnancy and the 6-month period after delivery. These samples were analyzed by several quantitative methods, including virus cultures of PBMCs and polymerase chain reaction (PCR) assays for HIV-1 RNA in plasma and DNA in PBMCs. The risk of transmission increased slightly with a higher viral load, but transmission and nontransmission occurred over the entire range of values for each assay. No threshold value of virus load was identified which discriminated between transmitters and nontransmitters. We also noted a significant rise in viral load and a decline in CD4+ lymphocytes in the six months after delivery. These findings suggest that a high maternal viral load is insufficient to fully explain vertical transmission of HIV-1. Additional studies are needed to examine the post-partum increase in viremia.

Anti-HIV Agents↗

PubMed2002

HIV-1 viral load and elevated serum alpha(1)-antichymotrypsin are independent predictors of body composition in pregnant Zimbabwean women.

Human immunodeficiency virus (HIV) infection affects body composition, but their relationship has not been studied in pregnant women. We conducted a cross-sectional study among 1669 women receiving antenatal care between 22 and 35 wk of gestation in Harare, Zimbabwe. The role of HIV-1 status and viral load, malaria and elevated serum alpha(1)-antichymotrypsin (ACT, an acute phase protein) in weight, body mass index (BMI), arm circumference (AC), triceps skinfold thickness (TSF), and arm muscle (AMA) and fat (AFA) area were assessed using multiple linear regression analysis. The mean (range) age was 24.4 (14-45) y and gestational age 29 (22-35) wk. HIV infection was present in 31.5% of the women, malaria parasitemia in 0.4% and 11.4% had serum ACT >0.4 g/L. There was no difference in any anthropometric variable between HIV-infected and uninfected women. However, women with viral loads (genome equivalents/mL) between 4 and 5 and >5 log(10) had 1.1 [95% confidence interval (CI): -0.3, 2.3] and 2.5 (95% CI: 0.1, 5.1) kg lower weights compared with uninfected women; this was explained by losses of both AFA and AMA. Malaria parasitemia was associated with 6 cm(2) (95% CI: 0.4; 11.8) or 25% lower AMA. Elevated serum ACT was a negative predictor of all anthropometric variables, i.e., levels between 0.3 and 0.4, 0.4 and 0.5 and >0.5 g/L were associated with 1, 2 and 6 kg lower mean body weights, respectively. Despite the limitations of a cross-sectional design, we conclude that arm fat and muscle areas, reflecting body fat and lean body mass, seem to be unaffected in the majority of HIV-infected pregnant women, but decline with increasing viral loads. The effects of viral load are not explained by elevated serum ACT, which is a strong independent predictor of all anthropometric variables.

Adolescent↗

PubMed2000

Reliability and validity of self-reported CD4 lymphocyte count and viral load test results in people living with HIV/AIDS.

Self-reporting is a common, convenient, and inexpensive method for collecting health status information in HIV/AIDS research, but the reliability and validity of these data remain suspect. HIV-positive persons (n=174) completed self-report measures of demographics, health status, and health literacy, and provided permission to collect CD4 cell counts and viral load results from provider charts. Clinically meaningful categories of CD4 cell counts were reliably and validly assessed using self-report measures. Self-reported viral load, however, demonstrated only marginally acceptable reliability and validity, with the greatest validity occurring for recall of undetectable viral load. Self-reported health status was most reliable and valid for persons with higher levels of education and literacy. CD4 cell counts can therefore be reliably and validly assessed through self-reporting, particularly when collected in clinically meaningful units from persons with higher education. Self-reported viral load should be interpreted with caution and is most reliable when dichotomized into detectable/undetectable categories.

Adult↗

PubMed1995

Pretreatment viral load and response to prolonged interferon-alpha course for chronic hepatitis C.

BACKGROUND/AIMS: We investigated the clinical benefit of long-term interferon therapy in chronic hepatitis C in relation to the pretreatment viral load and genotypes. METHODS: Chronic hepatitis C patients were randomly assigned to receive 28-week (n = 45) or 52-week (n = 43) courses of interferon-alpha. The responses were correlated with pretreatment viremic levels assessed by a branched DNA assay and genotypes. RESULTS: After the 28-week interferon-alpha course, sustained aminotransferase normalization showed correlation with a lower initial viral load. The normalization was achieved by 78% (7/9) of the low viremic (branched DNA-negative) patients, but only 22% (8/36) of the highly viremic (branched DNA-positive) patients (p < 0.01). Treatment with the 52-week interferon-alpha course increased the incidence of a sustained response in highly viremic patients and led to a decrease in relapse after therapy withdrawal (p < 0.05). Thus, 75% (6/8) of the low viremic patients and 49% (17/35) of the highly viremic patients showed a sustained response. The data further showed that frequent sustained responses in patients with genotypes III and IV were associated with a low initial viral load. CONCLUSIONS: These findings suggest that although the pretreatment viral load is an important virological factor for predicting responses to interferon in chronic hepatitis C, relapse in highly viremic patients may be prevented by long-term therapy.

Adult↗

PubMed2005

Changes in HIV RNA viral load, CD4+ T-cell counts, and levels of immune activation markers associated with anti-tuberculosis therapy and cotrimoxazole prophylaxis among HIV-infected tuberculosis patients in Abidjan, Cote d'Ivoire.

We analyzed changes in plasma human immunodeficiency virus (HIV)-1 viral load, CD4+ T-cell count, and markers of immune activation markers at start of treatment of tuberculosis and 12 months after among 44 HIV-1-infected patients with newly diagnosed, sputum-smear positive for Mycobacterium tuberculosis pulmonary infection. All patients received a standard regimen of 6 months of rifampicin and isoniazid with first 2 months of pyrazinamid with or without cotrimoxazole. Compared with values at start of treatment, median viral load increased by a median of 0.64 log10 copies/ml after 12 months of follow-up (P=0.0002). Median CD4+ T-cell counts were 393 cells/L at start of treatment and 370 cells/L after 12 months of follow-up (P=0.61). Levels of serum activation markers decreased significantly at 12 months of follow-up of the patients for both patients on standard and cotrimoxazole treatment. Levels of viral load, CD4+ T-cell counts, and markers of immune activation were not different for patients on standard treatment of tuberculosis compared with those on standard and cotrimoxazole treatment. Levels of serum activation markers decreased significantly at 12 months of follow-up of the patients for both patients on standard and cotrimoxazole treatment. Because viral load is a predictor of disease progression, its persistent elevated levels in blood of HIV-infected patients co-infected with tuberculosis, who successfully complete TB treatment, may account for the high mortality observed in this population.

AIDS-Related Opportunistic Infections↗

PubMed2002

Health care industries' perspective of viral load assays: the VERSANT HIV-1 RNA 3.0 assay.

This article will compare the VERSANT HIV-1 RNA 3.0 (bDNA 3.0) assay with other HIV-1 viral load assays, particularly the AMPLICOR HIV-1 MONITOR (Amplicor 1.5), the industry standard. The discussion will cover the history of viral load assay development and challenges to the field. It will finish with a description of the evolving markets for viral load assays in the developing world and the impact of variations in the different assays on their ability to reach those markets and patient populations.

Automation↗