Human Immunodeficiency Virus P24 Research Articles

Safety and tolerance of dideoxycytidine as a single agent: Results of early-phase studies in patients with acquired immunodeficiency syndrome (AIDS) or advanced AIDS-related complex

Phase I and II clinical studies have been conducted to test the safety and potential activity of the reverse transcriptase inhibitor, dideoxycytidine (ddC), in treating human immunodeficiency virus-1-infected patients. Although ddC appears to be active in combating viral infection, as judged by its ability to decrease human immunodeficiency virus-1 p24 antigen titers and increase the number of CD4 + lymphocytes, it is also capable of causing severe peripheral neuropathy in adose-dependent manner. The studies discussed here indicate that low-dose ddC treatment regimens substantially reduce the toxic side effects of this drug, and yet retain the ability to affect p24 antigen and CD4 + lymphocyte levels. These studies also define the window of therapeutic usefulness for ddC, and suggest that both safety and activity can be maintained during long-term, low-dose use of ddC.

Beta-Interferon Therapy in Patients with Poor-Prognosis Kaposi Sarcoma Related to the Acquired Immunodeficiency Syndrome (AIDS)

To study the efficacy of high doses of beta-ser-interferon (recombinant human 17-serine beta-interferon) in patients with human immunodeficiency virus (HIV) infection and Kaposi sarcoma. A nonrandomized, controlled trial of two high-dose regimens of beta-ser-interferon administered until tumor progression, toxicity, or an acquired immunodeficiency syndrome (AIDS)-defining opportunistic infection occurred. An AIDS treatment clinic at a tertiary care center. A sequential sample of 39 patients with biopsy-proven, AIDS-related Kaposi sarcoma were enrolled during a 2-year period. Thirty-eight patients were evaluable for response. Most patients (35 of 38) had one or more of the following clinical or laboratory predictors for a poor response to interferon therapy: HIV p24 antigenemia, low CD4 cell numbers, elevated beta 2-microglobulin levels, previous opportunistic infections, or previous systemic chemotherapy. Beta-ser-interferon was self-administered subcutaneously at home 5 days per week. The first 21 patients used 90 million IU/d, and the remainder used 180 million IU/d. Six patients (16%) had a major clinical response, and 15 (39%) had stable disease for prolonged periods. Toxicities were minimal; the major toxicity was a skin reaction at the injection site. The HIV p24 antigen level declined more than 50% in 8 of the 19 patients with initial values greater than 50 pg/mL. Antiretroviral activity and antitumor activity were seen only in patients with normal initial beta 2-microglobulin levels. Minimal changes were seen in CD4 and CD8 cell numbers. Only 1 patient had an opportunistic infection while on study, but five other patients developed infections after treatment was discontinued for an incidence of six opportunistic infections in 285 patient-observation months. The high doses of interferon did not improve the major response rate in patients with poor-prognosis, AIDS-related Kaposi sarcoma. There was, however, a suggestion of antiviral activity in patients with normal beta 2-microglobulin levels and a decrease in the expected incidence of opportunistic infections.

Human immunodeficiency virus (HIV) envelope and core proteins in CNS tissues of patients with the acquired immune deficiency syndrome (AIDS)

Frequency, cellular tropism and relation to pathology of productive infection with human immunodeficiency virus (HIV) in human central nervous system (CNS) were studied. Serial sections of formol-fixed and paraffin-embedded CNS tissues from 70 patients (69 with acquired immune deficiency syndrome, AIDS) were immunolabeled with monoclonal antibodies against HIV antigens (Ags) p17, p24, and gp41. Additional and double (immuno)stains were used to identify cell types and opportunistic infectious agents. HIV Ags were detected in 52 cases; they were restricted to cells with characteristics of microglia or macrophages. Anti-gp41, anti-p24, and anti-p17 labeled 50, 33, and 15 cases, respectively. Immunoreactivity for core proteins predominated in mature macrophages and microglia of fully developed lesions; additional immunoreactivity for gp41 was seen in microglia adjacent to, or unassociated with, histopathological lesions. Multifocal and/or diffuse lesions previously suggested as HIV induced because of characteristic histopathology, consistently contained large numbers of cells with HIV Ags (33 cases), confirming their HIV specificity. Isolated labeled microglia without associated pathology, found in seven brains, presumably represent the earliest stage of productive CNS infection by HIV. Lesions of opportunistic infections contained no (34 cases), few (16 cases), or many (4 cases) cells with HIV Ags. These data do not suggest transactivation of local HIV production by opportunistic agents as a frequent event in vivo. Development of specific HIV histopathology appears correlated with the number of productively infected cells.

Association of human immunodeficiency virus (HIV) p24 antigenemia with decrease in CD4 + lymphocytes and onset of acquired immunodeficiency syndrome during the early phase of HIV infection : Rinaldo C, Kingsley L, Neumann J, et al: J Clin Microbiol 27:880–884, 1989

Association of human immunodeficiency virus (HIV) p24 antigenemia with decrease in CD4 + lymphocytes and onset of acquired immunodeficiency syndrome during the early phase of HIV infection : Rinaldo C, Kingsley L, Neumann J, et al: J Clin Microbiol 27:880–884, 1989

Recombinant Soluble CD4 Therapy in Patients with the Acquired Immunodeficiency Syndrome (AIDS) and AIDS-Related Complex

To study the safety and pharmacokinetics and to derive preliminary evidence on surrogate indicators of efficacy of recombinant soluble CD4 (rsCD4) in patients with the acquired immunodeficiency syndrome (AIDS) and advanced AIDS-related complex. Open label, escalating dosage, phase I-II tolerance trial. Massachusetts General Hospital, Cedars-Sinai Medical Center, and Stanford University Medical School, three tertiary care institutions and members of the National Institute of Allergy and Infectious Diseases AIDS Clinical Trials Group. Cohorts of 3 to 11 patients received rsCD4 by intravenous infusion or intramuscular injection in dosages of up to 30 mg per day for 28 days. Recombinant soluble CD4 was tolerated by these patients with no significant clinical or immunologic toxicities. Serum levels of rsCD4 in patients receiving doses of 9 or 30 mg per day administered intramuscularly were in the range of rsCD4 concentrations required to inhibit replication of human immunodeficiency virus 1 (HIV-1) in vitro. A decline in serum HIV-1 p24 antigen was seen in patients receiving 30 mg of rsCD4 daily, but no such changes were noted at lower dosages. Recombinant soluble CD4 is well tolerated by patients with AIDS or advanced AIDS-related complex. Our study has also provided preliminary evidence of antiviral activity of rsCD4 in vivo. Our data suggest that further trials of receptor-based therapies against HIV-1 are warranted.

Human Immunodeficiency Virus (HIV) and Epstein-Barr Virus (EBV) Antigens and Genome in Lymph Nodes of HIV-Positive Patients Affected by Persistent Generalized Lymphadenopathy (PGL)

The presence of human immunodeficiency virus (HIV) and Epstein-Barr virus (EBV) antigens and genome has been investigated in 50 lymph nodes involved by persistent generalized lymphadenopathy (PGL). All the patients were HIV infected and most of them (42 of 50) also had anti-EBV serum antibodies. At lymph node level, HIV and EBV antigens were studied by immunohistochemistry using monoclonal antibodies directed against viral core proteins. The HIV p24 protein was detected in 43 of 50 lymph nodes within the B-cell germinal centers with a reticular pattern. Few cells with positive results for EBV antigens were found in only 2 of 50 lymph nodes. These rare EBV-positive centrocyte-like cells were mainly located in the germinal centers. The presence of HIV and EBV genome was also studied in lymph nodes involved by PGL, with the use of in situ and Southern blot hybridization. A positive reaction for HIV genome was detected in only 1 of 14 lymph nodes with the Southern blot hybridization, and the presence of EBV genome was never demonstrated in these lymph nodes with the use of both in situ and Southern blot hybridization. The expression of EBV antigens and genome was also investigated in the peripheral blood of 15 patients with PGL in which cells with positive results for EBV antigens were detected in a single case with a frequency of 1 X 10(-4). No evidence of EBV genome was found with the use of the in situ hybridization. These results suggest that EBV is not present in lymph nodes during the PGL phase and that its possible implication in the pathogenesis of acquired immune deficiency syndrome (AIDS)-associated lymphoma might be a late event.

Recombinant Human Interferon-β Suppresses the Replication of HIV and Acts Synergistically with AZT

The in vitro effects of recombinant human interferon-beta ser (rIFN-beta ser) and 3'-azido-3'-deoxythymidine (AZT) alone and in combination on human immunodeficiency virus (HIV) replication were examined. rIFN-beta ser inhibited HIV progeny virus synthesis in cell cultures chronically infected with HIV. When used in combination, suboptimally effective concentrations of rIFN-beta ser and AZT synergistically inhibited HIV-mediated syncytium formation in HeLa T4 cell cultures. Whereas AZT alone reduced HIV replication in human MT-2 cells, addition of low concentrations of rIFN-beta ser reduced by 4- to 1,000-fold the amount of AZT required to maximally block HIV p24 antigen synthesis and HIV-mediated cell lysis. No drug-related cytoxicity was observed when the two agents were used together at and above maximally effective concentrations. These results suggest that a safer, yet effective, therapy for HIV infections may be achieved with reduced doses of AZT in combination with rIFN-beta ser.

Effects of alcohol ingestion on in vitro susceptibility of peripheral blood mononuclear cells to infection with HIV and of selected T-cell functions.

A role for the biological effects of alcohol is postulated in the increased risk of AIDS known to be associated with chronic alcohol abuse and alcohol consumption during sexual activity. In pilot experiments peripheral blood mononuclear cells from healthy volunteers were studied before and after a single ingestion of 0.7 to 3.1 liters of beer or an equivalent dose of ethanol in other beverages. After moderate alcohol consumption there was increased human immunodeficiency virus (HIV) replication in peripheral blood mononuclear cells during 28 days of culture without mitogen stimulation as indicated by overnight syncytium formation with SUP-T1 indicator cells and by increased levels of HIV p24 antigen in the culture supernates. There was also decreased ability of lymphocytes to produce interleukin 2 and soluble immune response suppressor activity after stimulation with concanavalin A, the former, possibly both, for over 4 days after alcohol ingestion. These preliminary data extend well-known immunosuppressive effects of chronic alcohol ingestion to acute ingestion and raise the question: Could even casual alcohol consumption enhance HIV infectivity and/or enhance the progression of latent HIV infection?

Use of TrpE/Gag fusion proteins to characterize immunoreactive domains on the human immunodeficiency virus type 1 core protein

The human immunodeficiency virus (HIV) p24 core protein is one of the most immunogenic of HIV structural proteins. Infected individuals develop high titers of antibodies against p24 early in infection, which makes anti-p24 antibodies important serological markers. However, despite the clinical importance of the anti-p24 response, no systematic study to characterize the antigenic domains on the p24 protein has been reported. We report here on the use of 12 overlapping fragments of the HIV type 1 p24 protein, synthesized in bacteria as TrpE/Gag fusion proteins, to identify at least two and possibly three antigenic domains on the p24 protein. In addition, we note that different HIV-seropositive sera exhibited different patterns of reactivity with the p24 domains presented on our fusion proteins.

Isolation of human immunodeficiency virus from genital ulcers in Nairobi prostitutes.

Recent epidemiologic studies have implicated genital/anorectal ulcer disease as an important cofactor for acquisition and transmission of human immunodeficiency virus (HIV) during sexual intercourse. To better understand the mechanism for the association between genital ulcers and HIV, exudates from 62 genital ulcers of 56 HIV-seropositive prostitutes in Nairobi (Kenya) were cultured for HIV. Twenty-six ulcer cultures could not be evaluated for the presence of HIV because of bacterial or fungal contamination. HIV was isolated from 4 (11%) of the 36 remaining uncontaminated ulcer cultures (2 introital, 1 vaginal, and 1 cervical) from 4 separate women. HIV was isolated from the cervical os from only 2 of the 4 women. HIV p24 antigen was detected in exudate from 1 of the 4 culture-positive ulcers and 0 of 32 culture-negative ulcers. Genital ulcers in seropositive patients should be regarded as potential sources of HIV, which could be important in transmission of HIV during intercourse. Public health measures aimed at controlling sexually transmitted genital ulcer diseases should be an integral part of acquired immunodeficiency syndrome (AIDS) prevention programs.

In Vivo Activity Against HIV and Favorable Toxicity Profile of 2′,3′-Dideoxyinosine

The purine analog 2',3'-dideoxyinosine (ddI), which has anti-retroviral activity in vitro was administered for up to 42 weeks to 26 patients with acquired immunodeficiency syndrome (AIDS) or severe AIDS-related complex (ARC). Ten of these individuals were AZT-intolerant. Eight dose regimens were studied. The drug was orally bioavailable and penetrated into the cerebrospinal fluid (CSF). Comparatively little evidence of an effect against human immunodeficiency virus (HIV) was seen at the lowest four doses. However, patients in the four highest dose groups (ddI at 1.6 milligrams per kilogram intravenously and then greater than or equal to 3.2 milligrams per kilogram orally at least every 12 hours or higher) had increases in their circulating CD4+ T cells (P less than 0.0005), increased CD4/CD8 T cell ratios (P less than 0.01), and, where evaluable, more than an 80% decrease in serum HIV p24 antigen (P less than 0.05). The patients also had evidence of improved immunologic function, had reduced viremic symptomatology, and gained a mean of 1.6 kilogram with these comparatively infrequent dosing schedules (every 8 or 12 hours). The most notable adverse effects directly attributable to ddI administration at the doses used in this study included increases in serum uric acid (due to hypoxanthine release) and mild headaches and insomnia. These results suggest that serious short-term toxicity at therapeutic doses is not an inherent feature in the profile of agents with clinical anti-HIV activity. Further controlled studies to define the safety and efficacy of this agent may be worth considering.

Detection and subtyping of HIV-1 isolates with a panel of characterized monoclonal antibodies to HIV p24 gag

A panel of monoclonal antibodies (Mabs) was used to analyze the number and localization of B-cell epitopes on human immunodeficiency virus (HIV) p24 gag and the variability of these epitopes in sequential HIV isolates and in isolates from different geographical origin. The specificity of these Mabs was demonstrated by immunoblotting and radioimmunoprecipitation assays. Cross-inhibition experiments indicated the presence of at least five different epitopes on p24. Analysis with p24 recombinant products revealed that three of the Mabs to p24 were directed to epitopes localized on the C-terminal part. Four other Mabs were directed to epitopes localized on the N-terminal half of the protein. Anti-p24 Mabs were used to develop HIV p24 antigen-capture assays. Application of these assays in HIV isolation resulted in more efficient recovery of HIV. Serotyping of HIV-1 isolates with five anti-p24 Mabs demonstrated that 55 65 isolates recovered from Dutch and Belgian individuals, but only 4 9 HIV-1 African isolates, were recognized by all five Mabs. Five of nine Central African HIV-1 isolates were not reactive with at least one of these Mabs. The variability of p24 appeared to be predominantly localized on the N-terminal part of the protein. Lack of expression of antigenic determinants on p24 was shown to be independent of culture conditions. Moreover, an infectious molecular clone was shown to have the same serotype as the corresponding HIV isolate. The serotype of sequential isolates obtained from 17 individuals over a 1 1 2 to 2 1 2 - year period did not change, suggesting a limited in vivo p24 variation over time.

Association of Human Immunodeficiency Virus (HIV) p24 Antigenemia with Decrease in CD4 + Lymphocytes and Onset of Acquired Immunodeficiency Syndrome during the Early Phase of HIV Infection

Association of Human Immunodeficiency Virus (HIV) p24 Antigenemia with Decrease in CD4 ⁺ Lymphocytes and Onset of Acquired Immunodeficiency Syndrome during the Early Phase of HIV Infection

Predictive Markers for the Acquired Immunodeficiency Syndrome (AIDS) in Hemophiliacs: Persistence of p24 Antigen and Low T4 Cell Count

To investigate the predictive value of assays for human immunodeficiency virus (HIV) p24 antigen, p24 antibody, and gp120 antibody compared with T4 cell counts. Prospective cohort selected from persons who had HIV-antibody seroconversion. Eighty-seven persons with hemophilia with an actuarial cumulative acquired immunodeficiency syndrome (AIDS) incidence of 26% (CI, 12% to 40%), 8 years after HIV-antibody seroconversion. None. Human immunodeficiency virus p24 antigen was detected in 8 of 74 (11%) of the patients without AIDS and 7 of 13 (54%) of the patients with AIDS. The 2-year actuarial incidence of AIDS was 24% (CI, 0% to 48%) after detection of p24 antigen, 16% (CI, 0% to 34%) after loss of p24 antibody, 20% (CI, 0% to 45%) after loss of gp120 antibody, 31% (CI, 15% to 47%) after a T4 count of less than 200 cells/microL, and 67% (CI, 31% to 100%) after a T4 count of less than 200 cells/microL among those patients positive for p24 antigen. Very low numbers of T4 and T8 lymphocytes, presence of p24 antigen in serum, and absence of p24 antibody all had some predictive value. However, only p24 antigen (relative hazard 6.0, P = 0.008) and T4 counts (relative hazard 5.3, P = 0.002 with T4 count less than 200 cells/microL) independently predicted AIDS up to 12 months before diagnosis. Strong predictors of AIDS are p24 antigenemia or low T4 counts. Detection of p24 antigen is highly specific and complementary to the greater sensitivity of low T4 counts. These findings have important implications regarding prognosis, counseling, and the planning of clinical trials.

Serum 2-Microglobulin Decreases in Patients with AIDS or ARC Treated with Azidothymidine

Abnormally elevated serum beta 2-microglobulin has been associated with progression of human immunodeficiency virus (HIV) disease and could reflect in vivo HIV activity. We prospectively studied the effect of azidothymidine therapy on serum beta 2-microglobulin concentration in 41 patients with AIDS or AIDS-related complex. Median beta 2-microglobulin concentration decreased from 4.02 mg/L before therapy to 3.73 mg/L at week 24 of therapy (P = .016). Individual changes in beta 2-microglobulin during azidothymidine therapy correlated with changes in serum HIV p24 antigen (Spearman, r = .42, P = .007). Also, in a randomized placebo-controlled study, median beta 2-microglobulin concentration decreased after 16 w of therapy in 5 azidothymidine-treated patients compared with levels in 7 placebo-treated controls (P = .05). Serum beta 2-microglobulin appears to be a sensitive marker for in vivo antiretroviral drug activity and may be a better marker than serum p24 antigen for early intervention trials involving antiretroviral agents.

Progression to AIDS in patients with lymphadenopathy or AIDS-related complex: reappraisal of risk and predictive factors

purpose: In 1985, we reported that acquired immunodeficiency syndrome (AIDS) developed in 14 of 81 (17%) men with generalized lymphadenopathy followed prospectively for an average of 13 months. The presence of oral thrush or constitutional symptoms, or both, or severely impaired T4 + cell responses to specific antigen (interferon-gamma production) accurately identified patients at immediate risk for AIDS. The purpose of the current report is to describe the progress of these 81 patients during the three and a half years since enrollment and to include new data on initial serum levels of beta 2 microglobulin and human immunodeficiency virus (HIV) p24 antigen. patients and methods: The mean age of the 81 patients was 35.4 years; 79 were homosexuals and two were drug abusers. Immunologic testing was performed once at the time of enrollment in all patients. Seventy-seven of the 81 patients were sero-positive for HIV antibody. Frozen samples of serum, also obtained at initial study, were assayed in 1988 for beta 2 microglobulin and HIV p24 antigen. The clinical status of patients was determined six, 14, and 36 months after enrollment was closed (June 1984) by either interview and examination or telephone contact with private physicians. results: After three and a half years of follow-up, 42 patients have developed AIDS, including (1) 77% who had had thrush or symptoms, or both, (2) 80% to 88% of those who originally demonstrated marked immunologic abnormalities (skin test anergy, less than 200 T4 + cells/mm 3, T4/T8 cell ratio of less than 0.5, severely impaired interferon-gamma production [less than 25 U/mL], or elevated serum beta 2 microglobulin level [greater than 3.0 mg/L], and (3) 95% of patients with HIV p24 antigenemia. However, AIDS also developed in 51% of patients who had had more apparently benign initial manifestations (lymphadenopathy alone, herpes zoster), in 41% to 54% despite normal initial results for either T4 + cell number, interferon-gamma secretion, beta 2 microglobulin, or skin testing, and in 44% of those whose sera did not contain HIV antigen. conclusion: These updated results demonstrate the remarkably poor prognosis of patients with generalized lymphadenopathy or AIDS-related complex irrespective of initial clinical, immunologic, and serologic findings, and suggest that essentially all such persons may be candidates for antiviral therapy.

Association of human immunodeficiency virus (HIV) p24 antigenemia with decrease in CD4+ lymphocytes and onset of acquired immunodeficiency syndrome during the early phase of HIV infection

Human immunodeficiency virus (HIV) p24 antigenemia was assessed in a longitudinal study of 52 homosexual men who developed serum antibody to HIV. Antibody seroconversion to HIV as defined by a positive HIV enzyme immunoassay (EIA) confirmed by Western (immuno-) blot was associated with three major patterns of HIV antigenemia. In the first pattern, a transient antigenemia was noted 6 (six subjects) and 12 (one subject) months prior to detection of antibody by HIV EIA and Western blot in 7 (13.5%) of the 52 men. Use of an EIA employing a recombinant envelope protein (ENV9) was able to detect antibody in four of these seven men at the time of this early antigenemia. In the second pattern, HIV p24 antigenemia occurred in 8 (15.4%) of the 52 subjects within the first 12 months after HIV antibody seroconversion. No p24 antigen was detected in the 37 (71.1%) remaining subjects. CD4+ cell numbers were lower in antigen-positive men before and after antibody seroconversion. Development of acquired immunodeficiency syndrome (AIDS) or AIDS-related complex was strongly associated with evidence of persistent p24 antigenemia during the early, postseroconversion period. HIV p24 antigenemia may be of value in determining appropriate cohorts for drug therapy trials for subjects with early-phase HIV infection.

Investigation of atypical western blot (immunoblot) reactivity involving core proteins of human immunodeficiency virus type

Serum specimens which originally exhibited a narrow (indeterminate) 24-kilodalton core protein (p24) or p24/p55 pattern of reactivity with human immunodeficiency virus (HIV) in the Western blot (immunoblot) test were studied to gather information on antibody specificity. A total of 12 specimens were initially reevaluated with an indirect immunofluorescence assay (IFA), three enzyme-linked immunosorbent assays (ELISAs), and Western blot analyses. Five of the specimens were IFA positive and contained anti-gp160/gp120 antibodies which were observed only when an HIV Western blot antigen rich in gp160 and gp120 was used. The remaining seven serum specimens were nonreactive by IFA and showed variable reactivity in HIV antibody ELISAs. The specimens did not cross-react with core antigens for human T-cell leukemia virus types 1 and 2 or contain detectable levels of HIV p24 antigen. The p24/p55 reactivity of six of the seven indeterminate specimens could be reduced or eliminated by preincubating the specimens with disrupted, HIV-infected H9 cells but not with uninfected H9 cells. The six specimens also exhibited discernible reactivity with recombinant HIV p24 antigen. When an additional 23 indeterminate specimens were assayed, all of the serum specimens were nonreactive by IFA while 65% (15 of 23) showed various degrees of reactivity with the recombinant p24 protein. There was no indication that any of the HIV core antibody reactivity was caused by HIV infection. Indeterminate results for five patients with specific p24 reactivity, who were retested after a period of weeks or months, remained indeterminate for HIV antibody with no significant change in ELISA or Western blot reactivity.

Anti-HIV compound assessment by two novel high capacity assays

Two novel, semi-automated assays for the assessment of compounds for activity against human immunodeficiency virus (HIV) are described. One assay uses quantitation of DNA by fluorescence to monitor reversal by test compounds of HIV-induced growth inhibition. The second assay measures the amount of HIV p24 by an indirect immunofluorescent technique. Both assays are sufficiently sensitive to allow multiple sampling of 96-well plates. Intra- and inter-assay variability were within acceptable limits. The two assays provide comparable results for given compounds. Retrovir ® (3'-azido, 3'-deoxythymidine, AZT) protected MT4 cells from HIV-induced growth inhibition, and inhibited the production of HIV p24. Consistent with the results of others, the anti-HIV potency of AZT was dependent on the concentration of the infecting virus. Interestingly, AZT-protected, HIV-infected MT4 cells grew faster than mock-infected MT4 cells, and inclusion of Interleukin 2 in the assay eliminated this effect.

A possible homology between immunodeficiency virus p24 core protein and picornaviral VP2 coat protein: prediction of HIV p24 antigenic sites.

With the use of a sensitive sequence comparison algorithm, a homology has been suggested between the primary structures of simian immunodeficiency virus (SIV) p24 core protein and foot-and-mouth disease virus (FMD) VP2 coat protein. Since the FMD sequence is homologous to picornaviral VP2 sequences with known three-dimensional architecture and since the SIV p24 sequence can be convincingly aligned with that from human immunodeficiency virus (HIV), it was possible to predict an eight-stranded beta-barrel fold for the HIV core protein. From analogy with the known environments of the picornaviral coats, p24 sequence spans could be predicted as likely candidates for antibody attachment. These suggestions may be important for development of an AIDS vaccine.