Plasma P24 Antigen Research Articles

Seroprevalence and Risk Factors Associated with Human Immunodeficiency Virus Infection Type 1 in Donors of the National Blood Transfusion Center of Libreville (Gabon)

Background: Transmission of HIV through blood transfusion remains a public health problem, particularly in countries in Sub-Saharan Africa. However, no study has determined the epidemiological data regarding HIV-1 infection in Gabonese blood donors. The objective of this study is to assess the seroprevalence of HIV-1 and the risk factors associated with infection in donors from the National Blood Transfusion Center in Libreville (Gabon).
 Methods: A cross-sectional study carried out from June to August 2020 in 3669 persons donating blood at the National Blood Transfusion Center (NBTC). The ELISA technique (Evolis®, BioRad), the chemiluminescence technique (Cobas® e601, Roche), and the SD Bioline® HIV 1/2 test (Standard Diagnostics. Inc) were used for the detection of anti-HIV-1/2 antibodies and P24 antigen in donor plasma. Data were analyzed using SPSS software version 21.0, with p˂.05 considered statistically significant. 
 Results: The seropositivity rate HIV-1 was 0.8% (30/3669) (95% CI: 0.5; 1.1). The study was composed of 79.4% men and 20.6% women. The most representative age group was of 25-34 years with 54.5%. The seropositivity of men, women, and unrelated voluntary donors was 0.7%, 1.2%, and 1.0%, respectively. The risk factors such as the first blood donation (Adjusted Odds Ratio (AOR) = 0.1 [0.0 ;0.4], P= .002), multiple sexual partners (AOR = 6.2 [2.2;17.2], P= .001), primary educational level (AOR = 10.1 [1.4;75], P = .024), and dental care (AOR = 3.6 [1.2;11], P = .024) were significantly associated with HIV infection. About 0.14% of the patients had co-infection.
 Conclusion: In the Gabonese context, about one out of a hundred blood donors are HIV-infected. These carriers of HIV infection in the blood banks are mainly new donors with multiple sexual partners, limited education, and poor dental care.

Prediction of extended high viremia among newly HIV-1-infected persons in sub-Saharan Africa.

ObjectivePrompt identification of newly HIV-infected persons, particularly those who are most at risk of extended high viremia (EHV), allows important clinical and transmission prevention benefits. We sought to determine whether EHV could be predicted during early HIV infection (EHI) from clinical, demographic, and laboratory indicators in a large HIV-1 incidence study in Africa.DesignAdults acquiring HIV-1 infection were enrolled in an EHI study assessing acute retroviral syndrome (ARS) symptoms and viral dynamics.MethodsEstimated date of infection (EDI) was based on a positive plasma viral load or p24 antigen test prior to seroconversion, or the mid-point between negative and positive serological tests. EHV was defined as mean untreated viral load ≥5 log10 copies/ml 130–330 days post-EDI. We used logistic regression to develop risk score algorithms for predicting EHV based on sex, age, number of ARS symptoms, and CD4 and viral load at diagnosis.ResultsModels based on the full set of five predictors had excellent performance both in the full population (c-statistic = 0.80) and when confined to persons with each of three HIV-1 subtypes (c-statistic = 0.80–0.83 within subtypes A, C, and D). Reduced models containing only 2–4 predictors performed similarly. In a risk score algorithm based on the final full-population model, predictor scores were one for male sex and enrollment CD4<350 cells/mm3, and two for having enrollment viral load >4.9 log10 copies/ml. With a risk score cut-point of two, this algorithm was 85% sensitive (95% CI: 76%-91%) and 61% specific (55%-68%) in predicting EHV.ConclusionsSimple risk score algorithms can reliably identify persons with EHI in sub-Saharan Africa who are likely to sustain high viral loads if treatment is delayed. These algorithms may be useful for prioritizing intensified efforts around care linkage and retention, treatment initiation, adherence support, and partner services to optimize clinical and prevention outcomes.

Outcomes of acutely HIV-1-infected individuals following rapid antiretroviral therapy initiation.

Few data exist on the benefits and acceptability of rapid initiation of antiretroviral treatment in acute HIV infection (AHI). We analysed a large cohort of acutely infected HIV patients starting antiretroviral therapy (ART) to determine uptake, linkage into care and time to achieve viral suppression. Case notes of all individuals diagnosed with AHI between May 2014 and October 2015 at 56 Dean Street, a sexual health clinic in London, UK were reviewed. AHI was defined through documentation of plasma HIV RNA positivity only, plasma HIV RNA and p24 antigen positivity with a negative HIV enzyme immunoassay (EIA) test or HIV EIA test switching from negative to positive within 6 weeks. Between-group comparisons of time to viral suppression according to ART chosen were performed using the log-rank test. We identified 113 individuals with AHI. Linkage to care was 95%. 77% of patients started ART at first medical appointment: all men who have sex with men, median age 35 years, median viral load (VL) log10 6.45, median CD4+ T-cell count 483 cells/mm3. Median time from diagnosis to ART initiation was 20 days. At 24 weeks, no patients had discontinued ART; 99% of patients achieved viral suppression by 24 weeks, with a median time to documented VL suppression of 74 days. Viral suppression was more rapid with integrase inhibitors compared with other regimens (median 41 versus 88.5 days, P<0.05). In acute HIV infection, individuals demonstrated high ART uptake and rapid VL suppression suggesting that early treatment with antiretrovirals is acceptable and efficacious.

Presence of p24-Antigen Associated to Erythrocyte in HIV-Positive Individuals Even in Patients with Undetectable Plasma Viral Load

BackgroundHIV adherence to erythrocytes has been demonstrated in vitro, and it has been suggested that erythrocytes may be carriers of the virus. However, the association between HIV particles or viral proteins and erythrocytes in HIV-infected individuals is still to be elucidated.Methodology/Principal FindingsHIV-positive participants (n = 112) were classified into two groups according to values of three plasma viral loads (pVL) determined during the 12-month period prior to the study. The first group included 71 individuals with detectable pVL, whereas the second group included 41 individuals with undetectable pVL. Plasma viral load, erythrocyte-associated p24-antigen and p24-antigen in plasma were determined at the moment of the study. A total of 51 out of the 71 patients with detectable pVL showed erythrocyte-associated p24-antigen whereas 13 showed p24-antigen in plasma. Twenty-two out of the 51 patients with erythrocyte-associated p24-antigen showed pVL<10,000 copies/ml and undetectable p24-antigen in plasma. The data indicates that the amount of erythrocyte-associated p24-antigen was not related to p24-antigen in plasma or pVL levels in this group. Among the 41 patients with prior undetectable pVL, eight presented detectable pVL and erythrocyte-associated p24-antigen at the moment of the study. The other 33 showed undetectable pVL and five of these presented erythrocyte-associated p24-antigen. A positive relationship was found between the presence of erythrocyte-associated p24-antigen and the detectable pVL at the moment of the study (p<0.00001). Even more, in another series of assays, a detectable viral load associated to erythrocytes was determined and it was always accompanied by erythrocyte-associated p24-antigen detection.Conclusions/SignificanceThis study demonstrates the presence of erythrocyte-associated p24-antigen in HIV-infected individuals. Since erythrocyte-associated p24-antigen is not always related to pVL or p24-antigen in plasma, erythrocyte-associated p24-antigen showed viral expression not represented in plasma. Therefore, the determination of erythrocyte-associated p24-antigen may contribute to better understand the kinetics and/or evolution of HIV infection.

Centrifugation improves the detection of HIV-1 p24 antigen in plasma from children born to mothers infected with HIV-1

Detection of HIV proteins and/or nucleic acids is necessary for the diagnosis of perinatal HIV infection. Despite its low sensitivity, detection of p24 antigen in plasma is a simple and economic method for the diagnosis of HIV in exposed children. The aim of this study was to improve the sensitivity of detection of p24 using centrifugation of plasma. Forty-seven selected stored samples from 37 children (23 infected, 14 uninfected, median age of 137 days) were examined. Plasma samples (volume 0.3–1.5 ml) were defrosted, centrifuged at 23,500 × g at 4 °C for 60 min and determination of p24 was carried out in the resuspended pellet (0.12 ml). In 32 plasma samples from infected children, p24 was found originally in 6 (18.7%) and resulted positive in 24 (75%) pellets. When only one sample per child was considered, sensitivity was significantly higher in pellets, 3/23 uncentrifuged plasma samples and 15/23 pellets (McNemar Test, p < 0.001). Specificity was 100%. The absorbance/cut-off ratio was always higher in the pellets from positive children ( p = 0.028). Plasma samples with volumes of 1 ml or more achieved a higher sensitivity (91.7% vs. 36.4%, p = 0.009). Centrifugation of plasma samples prior to determination of p24 in pediatric patients resulted in a significant increase in sensitivity.

Adaptation of the Ultrasensitive HIV-1 p24 Antigen Assay to Dried Blood Spot Testing

Implementation of molecular tests for the assessment of pediatric HIV-1 infection in resource-limited countries is difficult because of technical complexity and costs. Alternatives like the ultrasensitive HIV-1 p24 antigen enzyme-linked immunosorbent assay have therefore been proposed. We have now adapted this test to dried blood spot (DBS) plasma p24 antigen (p24). High background activity was recognized as originating from endogenous peroxidase and eliminated by H2O2 quenching. The assay was evaluated with 72 pediatric specimens from Tanzania and with 210 pediatric or adult specimens from Switzerland. A real-time polymerase chain reaction assay for DBS DNA and/or plasma RNA identified HIV-1 infection in 38 Tanzanian children. HIV-1 subtypes included 18 C, 9 A1, 8 D, 1 AC, 1 J-like, and 1 unidentified. The detection rates for the different assays were as follows: DBS-p24, 32 (84%) of 38 samples; DBS DNA, 30 (79%) of 38 samples; plasma-p24, 23 (85%) of 27 samples; and plasma RNA, 30 (100%) of 30 samples. False-negative DBS-p24 was associated with subtype D (P < 0.01). DBS-p24 detection for non-D subtypes was 93% (95% confidence interval: 81% to 99%), and for subtype C, it was 94% (95% confidence interval: 76% to 99%). Specificity among 193 HIV-negative DBS samples was 100%. Correlation of DBS-p24 and plasma-p24 concentrations was excellent (R = 0.83, P < 0.0001). DBS-p24 is thus a promising alternative to molecular tests for HIV-1 in subtype C regions. It should now be evaluated in large studies of children for accurate assessment of diagnostic sensitivity.

Rhabdomyolyse aiguë associée à une primo-infection à VIH-1 : une nouvelle observation

Introduction Acute human immunodeficiency virus type 1 infection is a clinical and biological misleading and often undiagnosed illness. Laboratory studies frequently demonstrate abnormalities. Acute rhabdomyolysis is rarely reported. Exegesis Authors report the case of an African man who presented with acute fever, cough, diarrhea, conjunctivitis, thrombocytopenia, lymphopenia, and rhabdomyolysis without other possible cause. HIV test and detection of plasma p24 antigen were initially negative but were controlled positive and associated with high level of viral RNA. Conclusion Symptomatic primary human immunodeficiency virus infection presenting with acute rhabdomyolysis was diagnosed. Diagnosis of primary HIV-1 infection must be considered in young people and patients at risk who present with acute rhabdomyolysis and fever.

Comparative study on use of CD4 T cell count and plasma P24 antigen concentration in antiretroviral therapy monitoring for HIV/AIDs patients in Kano, Nigeria

Background Monitoring antiretroviral therapy through CD4T-cell count and viral load or reverse transcriptase assessment is used in developed countries. However, cost implication, demand of sophisticated equipments, high level manpower need made such technology impracticable in most of the African laboratory settings. Developing countries having the fewer specialized diagnostic facilities and more affected by the disease requires reliable and cost effective monitoring options (W.H.O., 2003). Research works carried out on various viral parameters such as p24 antigen, plasma RNA, rapid reverse transcriptase detection method were put into trials; p24 antigen emerged as the best possible option for African laboratories use (because of its simplicity and affordability) and correlates well with viral load and can be used as an alternative to viral load monitoring (Schupbach, et al., 2003).

The Use of Nanoarrays for Highly Sensitive and Selective Detection of Human Immunodeficiency Virus Type 1 in Plasma

Arrays of antibodies with well-defined feature size and spacing are necessary for developing highly sensitive and selective immunoassays to detect macromolecules in complex solutions. Here we report the application of nanometer-scale antibody array-based analysis to determine the presence of the human immunodeficiency virus type 1 (HIV-1) in blood samples. Dip-pen nanolithography (DPN) was used to generate nanoscale patterns of antibodies against the HIV-1 p24 antigen on a gold surface. Feature sizes were less than 100-nanometers, and the activity of the antibody was preserved. HIV-1 p24 antigen in plasma obtained directly from HIV-1-infected patients was hybridized to the antibody array in situ, and the bound protein was hybridized to a gold antibody-functionalized nanoparticle probe for signal enhancement. The nanoarray features in the three-component sandwich assay were confirmed by atomic force microscopy (AFM). Demonstration of measurable amounts of HIV-1 p24 antigen in plasma obtained from men with ...

Vaginal transmission of HIV-1 in hu-SCID mice: a new model for the evaluation of vaginal microbicides.

To develop an animal model of vaginal transmission of HIV-1 for the evaluation of vaginal microbicides. Vaginal infection was performed in SCID mice reconstituted with 4 x 107 human peripheral blood lymphocytes (hu-PBL) by non-invasive vaginal administration. The hu-PBL were previously infected in vitro with a non-syncytium (NSI) strain of HIV-1 (SF162) (hu-PBL-SCID). Lymphocyte migration in vivo was examined using fluorescently labelled human lymphocytes. The percentage of CD4 T cells, plasma viral load and p24 antigen were evaluated using fluorescent activated cell sorting (FACS), the Amplicor HIV-1 monitor kit and enzyme-linked immunosorbent assay, respectively. Polymerase chain reaction (PCR) analysis was performed on DNA extracted from spleen and lymph nodes. For in vivo migration of labelled lymphocytes, the mice were sacrificed after 4, 24 and 48 h; vaginae and local lymph nodes were removed, snap frozen with OCT, sectioned and examined by fluorescent microscopy and FACS. HIV transmission was established using virus-infected cells inoculated vaginally, as shown by FACS, HIV viral load, p24 and PCR results. Labelled cells were easily located within the vaginal tissues after 4 h. However, few or no cells could be identified after 24 or 48 h at the vaginal level, whereas labelled cells could be detected at the level of regional lymph nodes. Because of its simplicity and practical features compared with other animal models, the vaginal HIV-infected hu-SCID mouse model may prove useful to test the activity of compounds against cell-associated HIV and, possibly, other sexually transmitted diseases.

A complex human immunodeficiency virus type 1 A/G/J recombinant virus isolated from a seronegative patient with AIDS from Benin, West Africa.

A human immunodeficiency virus type 1 (HIV-1(B76)) originating from Benin (West Africa) was isolated and characterized. The patient had severe clinical AIDS and presented an unusual serological profile. Only one out of five different detection assays was able to demonstrate the presence of antibodies to HIV, whereas confirmatory assays remained indeterminate. In contrast, both plasma viral load and p24 antigen level were unusually high. HIV-1 infection was proved by viral RNA and proviral DNA amplification. HIV-1(B76) partially purified lysate reacted strongly with all anti-HIV-1-positive sera from the region but B76 plasma did not react with subtype A control viral antigen. This patient is likely to have had severe acquired immune dysfunction explaining her lack of immunological reactivity. Phylogenetic analysis of the genome identified a complex HIV-1 A/G/J recombinant. The gag and pol genes, and the majority of nef,are characteristic of subtype A; the gag/pol junction, the 3' end of pol, vpu and env genes were characteristic of subtype G; vif, vpr and the 5' end of nef were subtype J. In addition, part of the HIV-1(B76) genome had considerable sequence similarity with the previously described CRF06 cpx (BFP90) isolate. HIV-1(B76) did not exhibit any remarkable replication properties or cell tropism in vitro.

Hu-SCID: A model for the evaluation of vaginal microbicides

There is a need of new approaches to test and develop vaginal microbicides with antiviral specificity. We are studying a hu-SCID mouse animal model of vaginal transmission of HIV-1. Vaginal infection was performed using SCID mice reconstituted intraperitoneally with 3 × 107 human PBMC. At day 0 the mice were treated with 5mg of progestin and followed at day 7 by a non invasive vaginal administration of 1 × 106 PBMC previously infected in vitro with NSI stain of HIV-1. Systemic infection was investigated after two weeks post-inoculation collecting different samples: plasma, spleen cells, lymph-nodes cells, peritoneal cells and supernatants from lavage. Plasma viral load and p24 antigen detection were evaluated by using the amplicor HIV-1 monitor kit and cocoltivation, respectively. Polymerase chain reaction (PCR) analysis was performed on DNA extracted from tissues (spleen, lymph-nodes, peritoneal cells) to determine the presence of proviral copies using specific primers for HIV-1. In our experiments transmission was established using NSI virus infected cells inoculated vaginally as shown by either PCR results or plasma and peritoneal fluid viral load and p24 antigen detection. This hu-SCID mouse model may prove useful to test the activity of compounds against HIV and sexually transmitted diseases.

Effect of the HIV-1 syncytium-inducing phenotype on disease stage in vertically-infected children.

The syncytium-inducing (SI) capability of HIV-1 isolates from 48 HIV-infected children was determined in order to examine the association of the SI phenotype with an AIDS diagnosis and/or with other clinical parameters in HIV-infected children. In a retrospective cross-sectional analysis, phenotypic data were linked to clinical and immunologic data from each patient. Multiple longitudinal samples were analyzed from 14 patients. Children with SI viruses were older than children with nonsyncytium-inducing (NSI) strains. Twelve of 13 children less than 2 years old carried NSI viruses, seven of the 12 already had a diagnosis of AIDS. Two children under 2 years of age died within 1 month of NSI virus isolation. Although plasma p24 antigen levels tended to be higher in the NSI group, the difference appeared to reflect high p24 levels in children under 2 years old with AIDS. When children under 2 were omitted, differences in age, CD4+ cell counts, p24 antigenemia, and clinical parameters were not significant. The SI phenotype of HIV-1 did not occur more frequently in children with an AIDS diagnosis. Four children remained stable with SI isolates overtime periods of 16 to 31 months. Three children's isolates converted from NSI to SI and 2 converted from SI to NSI. These data indicate that SI viruses do not play a significant role in progression to AIDS during the first 2 years of life. Furthermore, for children above the age of 2, the association between advanced disease stage and the SI phenotype in adults may not apply.

Increased frequency of CCR-5 delta 32 heterozygotes among long-term non-progressors with HIV-1 infection. The Australian Long-Term Non-Progressor Study Group.

The beta-chemokine receptor CCR-5 is used as a coreceptor by macrophage-tropic strains of HIV-1 to gain entry into CD4+ cells. To determine the effect of a common 32 base-pair deletion mutation in the CCR-5 gene (CCR-5 delta 32) on progression of HIV infection to AIDS, and to assess the level of heterozygosity for this mutation in a well-defined group of long-term non-progressors (LTNP). Sixty-four HIV-1-infected LTNP (CD4+ T lymphocyte count > 500 x 10(6)/l after 8 years) were compared with 95 individuals infected within a similar period (1983-1986) but who had rapidly progressed to AIDS and death, and with a further 120 HIV-positive individuals with CD4+ counts < 500 x 10(6)/l. The presence of the CCR-5 delta 32 mutation was assessed using polymerase chain reaction with primers spanning the 32 base-pair deletion. CD4+ and CD8+ counts, plasma HIV-1 RNA, p24 antigen and beta 2-microglobulin levels in LTNP carrying the CCR-5 delta 32 mutation were compared with LTNP lacking the mutation. A marked increase in the frequency of CCR-5 delta 32 heterozygosity was found among LTNP (35.9%) compared with rapid progressors (12.6%; P = 0.0005) and patients selected on the basis of a CD4+ T-cell count < 500 x 10(6)/l (12.5%; P = 0.0004). LTNP heterozygous for CCR-5 delta 32 had a significantly higher CD8+ T-cell count than those without the mutation (1218 versus 972 x 10(6)/l; P = 0.044). No significant correlation was observed between heterozygosity and CD4 count, viral load, p24 antigen or beta 2-microglobulin within the LTNP group. This study provides the strongest evidence to date for the importance of a single copy of the CCR-5 delta 32 mutation in long-term non-progression of HIV infection, which may involve, in part, CD8+ T lymphocytes.

Correlation of ribonucleic acid polymerase chain reaction, acid dissociated p24 antigen, and neopterin with progression of disease: A retrospective, longitudinal study of vertically acquired human immunodeficiency virus type 1 infection in children

Objective: We investigated the relationship between cell-free viral load, neopterin, age-adjusted CD4 + cell concentration, and clinical events in 49 children with vertically acquired human immunodeficiency virus type 1 infection. Study design: Viral load was measured by quantitating viral ribonucleic acid in serum by polymerase chain reaction and measurement of immune complex dissociated p24 antigen in serum and plasma. Children were followed for an average of 2½ years, with an average of 6 samples per child. Medical records were reviewed for weight, CD4 + cell count, and clinical events. Results: High virus copy number in serum was predictive of a decrease in weight-for-age z score during the subsequent 6 months. High viral load, low CD4 + cell count, and high neopterin level were correlated with encephalopathy. High viral load correlated with opportunistic infections. All of these relationships held regardless of treatment status, although viral load decreased significantly after treatment was begun. Conclusions: Measurements of viral load were useful prognostic indicators for poor weight gain. Elevated serum virus levels and neopterin values and low CD4 + cell counts were all associated with encephalopathy. (J Pediatr 1997:130:898-905)

Cost-effectiveness of expanded human immunodeficiency virus-testing protocols for donated blood.

This study was designed to estimate the cost-effectiveness of expanding the human immunodeficiency virus (HIV)-testing protocol for donated blood beyond screening for HIV antibodies to further reduce the risk of HIV transmission through transfusion. A Markov decision analysis model was developed to estimate the cost-effectiveness of HIV antibody testing (at a cost of $5/unit) and of adding to that protocol a second HIV test, either plasma p24 antigen detection or RNA polymerase chain reaction (PCR) (at costs of $5/unit and $8/unit, respectively). Test efficacy was projected from anticipated window-period reductions (6 days for p24 antigen, 11 days for RNA PCR), and donor seroconversion rates were derived from the Retrovirus Epidemiology Donor Study. On the basis of current estimates of HIV prevalence rates in blood donors (1/10,000) and 16 million annual transfusions in the United States HIV antibody testing prevents 1568 cases of transfusion-acquired HIV infection each year at a cost of $3600 per quality-adjusted year of life saved. The addition of p24 antigen testing would prevent 8 more cases at a net additional cost of $60 million annually ($2.3 million/quality-adjusted life year); RNA PCR testing would prevent 16 more cases at a net additional cost of $96 million annually ($2.0 million/ quality-adjusted life year). Although expanding the donor HIV screening protocol with p24 antigen or RNA PCR testing will prevent rare cases of transfusion-associated HIV, the cost-effectiveness of such an addition is predicted to be far below that of most medical interventions. Thus, HIV test protocol additions are unlikely to provide cost-effective improvements to blood safety in the United States.

Human immunodeficiency virus type 1 activation after blood transfusion.

Anemia and transfusion are predictors of disease progression in AIDS patients. This study was designed to examine the effects of blood transfusion on human immunodeficiency virus type 1 (HIV-1) expression. Assays of plasma viral load were performed before and after transfusion in nine HIV-1-infected patients who required blood transfusion for refractory anemia. There was a modest rise in plasma HIV-1 p24 antigen and plasma HIV-1 RNA beginning 1 to 2 weeks after the blood transfusion. The mean change in plasma p24 antigen for all patients was 9.3 +/- 5.1 (mean +/- SE) pg per mL at Week 2 after transfusion and 18 +/- 11.1 pg per mL at Week 4. Plasma HIV-1 RNA levels were unchanged immediately after transfusion and exceeded pretransfusion levels with a mean rise of 84 +/- 40 percent (SE) at Week 1, 70 +/- 27 percent at Week 2, and 67 +/- 38 percent at Week 4 (p = 0.006, exact permutation test). There was no increase in spontaneous or interleukin 2-induced lymphocyte proliferation or p24 antigen production by patients' lymphocytes that were examined immediately after blood transfusion. The transfusion of blood to persons with advanced HIV-1 infection modestly increases plasma levels of HIV-1. The activation of HIV-1 expression by transfusion may help to explain the accelerated course of HIV-1 disease in recipients of blood transfusion.

Changes in Virus Load Markers during AIDS-Associated Opportunistic Diseases in Human Immunodeficiency Virus-Infected Persons

Human immunodeficiency virus (HIV) load markers are being used increasingly to monitor disease progression and evaluate antiretroviral therapy. This study examined plasma HIV RNA and p24 antigen levels before, during, and after 15 AIDS-associated opportunistic disease events in patients with AIDS (median CD4 cell count = 65/microL). Plasma HIV RNA was detected during 13 of the 15 events (median level before an event = 21,000 copies/mL). There was an increase in the level of plasma HIV RNA with the onset of an AIDS-associated opportunistic disease during 11 of 13 events for which HIV RNA was detectable (median level during an event = 145,000 copies/mL). There was a decline in the level of HIV RNA with the recovery from disease (median level after an event = 29,700 copies/mL). In contrast, there was no consistent or significant change in p24 antigen levels or CD4 cell counts with either the onset of or recovery from an event. Clinical interpretation of plasma HIV RNA changes must take into account this reversible elevation during AIDS-associated opportunistic disease.

Shortened survival in infants vertically infected with human immunodeficiency virus with elevated p24 antigenemia

Objective: To determine whether the amount of p24 antigenemia in the first 6 months of life is a predictor of survival in children infected vertically with human immunodeficiency virus type 1. Methods: A retrospective study of vertically infected infants and children who were followed prospectively from early infancy and who had quantitation of plasma p24 antigen concentration in the first 6 months of life. Infants were first stratified by duration of survival as infants who died before 2 years of age (short-term survivors) and infants who survived to 2 years of age (intermediate-term survivors). The median p24 antigen concentration and the proportion of infants in each group with high concentrations of antigen were compared. Analyses with and excluding all p24 determinations made after the use of antiretroviral agents were compared. Kaplan-Meier product limit analysis was used to compare survival in infants with low and high antigenemia during the first 6 months of life. Results: The median p24 antigen concentration in 15 short-term survivors was 228 pg/ml, compared with 14 pg/ml in 26 intermediate-term survivors ( p <0.05). The proportion of children with >100 pg/ml of p24 was higher in short-term than in intermediate-term survivors ( p = 0.01). Survival to 2 years of age in infants in whom all p24 antigen values during the first 6 months of life were 100 pg/ml or less was 91%, in comparison with 39% in infants with values greater than 100 pg/ml ( p = 0.0017). Conclusions: Elevated p24 antigenemia in the first 6 months of life is associated with shorter survival and may be a useful predictor of outcome. (J P EDIATR 1995;127:538-43)

Kinetics of detection of antibodies to HIV-1 and plasma p24 antigen during a severe primary HIV-1 infection

Kinetics of detection of antibodies to HIV-1 and plasma p24 antigen during a severe primary HIV-1 infection