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Biomedical subjects

M D Lairmore

Publications and source records attributed to M D Lairmore.

At least 55 records · Page 3Linked to original sources
PubMed1995

Evaluation of immunodominant epitopes of human T-lymphotropic virus type 1 (HTLV-I) using synthetic peptides.

Human T-lymphotropic virus type 1 (HTLV-I) causes adult T-cell leukemia/lymphoma (ATLL) and has been associated with a variety of immunologically-mediated diseases. Recently, the immunodominant epitopes of HTLV-I have begun to be defined through the utilization of synthetic peptides and recombinant proteins. Strategies to define the conformational features of immunogenic peptides and design chimeric and multivalent constructs that mimic native viral proteins have provided the opportunity to create an effective synthetic vaccine against HTLV-I infection. An ideal peptide vaccine to be universally immunogenic must incorporate rationally designed antigenic determinants that accurately mimic the corresponding structural architecture found in native proteins and elicit relevant components of the immune system. We have recently designed and tested chimeric and beta-sheet template constructs containing HTLV-I immunodominant peptide motifs that elicit neutralizing antibody responses and overcome genetically restricted immune responses. To further illustrate putative vaccine candidates, HTLV-I env and tax proteins were analyzed using various computer-predicted correlates of protein antigenicity, secondary structural predictions, and major histocompatibility complex class I binding motifs. These approaches provide the opportunity to design synthetic peptide vaccines against HTLV-I infection that are based on structurally defined criteria, as well as test the influence of glycosylation on peptide conformation and immunogenicity.

Amino Acid Sequence↗
PubMed1995

Immunogenicity and conformational properties of an N-linked glycosylated peptide epitope of human T-lymphotropic virus type 1 (HTLV-I).

The identification and characterization of epitopes of human T-lymphotropic virus type 1 (HTLV-I), which elicit an effective humoral or cell-mediated immune response, remains a central obstacle to the development of a peptide-based vaccine against the virus infection. The objective of the studies presented here was to examine the influence of N-linked glycosylation on peptide structure and immunogenicity. We engineered the 233-253 sequence of gp46 of HTLV-I to contain an N-acetylglucosamine (GlcNAc) residue at Asn244. Secondary structure prediction using computer algorithms indicated that this peptide may contain a beta-turn at residues 242-246. Recent work with model glycopeptides suggests that beta-turn conformation in peptides may be induced, and probably is stabilized, by the presence of even a single sugar residue. In the present study, the structures of the 233-253 peptide, SC1, and the 233-253(Asn244-GlcNAc) glycopeptide, SC2, were determined. Similar conformation was exhibited by both the glycosylated and nonglycosylated peptide displaying a beta-turn at residues 243-246 and extended-chain structure at the peptide/glycopeptide termini. Both peptides were engineered into chimeric constructs with a promiscuous T-cell epitope from measles virus and were used as immunogens in rabbits. Both chimeric peptides were highly immunogenic in rabbits, producing high-titered antibodies as early as primary + three weeks. The antibodies generated against either construct were able to bind to whole virus (ELISA) and to gp46 (radioimmunoprecipitation assay). Additionally, human sera of individuals known to be positive for HTLV-I recognized both the glycosylated and nonglycosylated constructs. It appears that the 233-253 peptide is able to adopt a conformation that mimics the structure in native gp46, and addition of a GlcNAc residue at Asn244 does not affect the conformational preference or stability of this construct; nor does glycosylation alter immunogenicity but instead appears to enhance immune recognition.

Amino Acid Sequence↗
PubMed1994

Effects of whole blood lysis and fixation on the infectivity of human T-lymphotropic virus type 1 (HTLV-I).

Whole blood lysis and fixation methods for flow cytometric (FCM) analysis were tested for their ability to reduce the infectivity of human T-lymphotropic virus type 1 (HTLV-I). Our goals were to: (1) determine the effects of 1.0 and 2.0% paraformaldehyde (PF) fixation on HTLV-I infected cell lines and (2) assess the infectivity of blood samples containing HTLV-I-infected cells following processing with 5 commercially available products (Immuno-lyse, ImmunoPrep/Q-Prep, FACS lysis solution, GenTrak lyse and fix reagent, and Ortho-mune lysing reagent) compared to ammonium chloride lysis with either 0.1 or 1.0% PF fixation. Infectivity was determined by monitoring HTLV-I p24 antigen production in cocultures of treated leukocytes with uninfected peripheral blood mononuclear cells (PBMC). Each method effectively reduced the viability of treated leukocytes. Commercial lysis/fixation methods significantly reduced HTLV-I infectivity compared to prepared ammonium chloride/PF-based methods. For all preparations, increasing the time of fixation (e.g., 60 min) effectively reduced viral infectivity. Taken together, these data suggest that commercially available fixatives greatly reduce, but do not eliminate the risk of HTLV-I infection during processing of viral-infected cells for FCM analysis.

Fixatives↗
PubMed1994

Differential replication and pathogenic effects of HIV-1 and HIV-2 in Macaca nemestrina.

OBJECTIVE: HIV-1 and HIV-2 isolates representing various geographic regions and distinct viral subtypes were examined for their ability to establish both in vitro and in vivo productive infections of Macaca nemestrina (pigtail macaque) peripheral blood mononuclear cells. METHODS: Animals were inoculated with either autologous cell-associated or cell-free viral preparations of selected isolates. HIV-specific immune responsiveness, hematologic changes, genetic variation, and virus burden were monitored as delineators of HIV pathogenesis. RESULTS: HIV-2 replication in vitro and in vivo correlated with nascent antigen production and rising viral titers as determined by infectious center assays. Infection was detectable by polymerase chain reaction amplification of proviral sequences in macaque cells as early as 1 week postinoculation. Two distinct patterns of CD4+ cell depletion induced by HIV-2 infection were observed during the first month postinoculation and characterized by a moderate loss sustained through 20 weeks postinoculation or a substantial loss maintained long-term (> 90 weeks). Identity between inoculating viral stocks and subsequent viral isolates from animals was established comparatively by limited sequence analysis of specific domains within the HIV-2 pol and env genes. In contrast, replication of HIV-1 isolates was limited or only semipermissive in vitro. Intravenous inoculation of HIV-1 field isolates, using conditions successful for HIV-2 (for example, identical viral titers), failed to establish a productive viral infection leading to seroconversion of fluctuations in hematologic cell markers. Infection with a high-titer inoculum of a laboratory-adapted HIV-1 strain in vivo, as demonstrated by polymerase chain reaction analysis, produced seroconversion in the absence of overt viral replication or hematologic variations in one out of four animals. CONCLUSIONS: This system provides for multifaceted modeling of HIV pathogenesis, primarily with HIV-2 and potentially with HIV-1/-2 chimerics, in support of immunotherapeutic developments and critical evaluation of intervention practices.

Amino Acid Sequence↗
PubMed1994

Sexual transmission of simian T-lymphotropic virus type I: a model of human T-lymphotropic virus type I infection.

Simian T-lymphotropic virus type-I (STLV-I) seronegative females placed together with seropositive males for breeding purposes were followed from 1984-1990 to determined seroconversion rates by enzyme immunoassay and western immunoblot analysis. Two of 26 females and 1 of 4 males previously negative for antibodies to STLV-I seroconverted during the study period. Statistical analysis of sexual encounters indicated that the probability of a seronegative female testing positive for STLV-I after a sexual encounter with a seropositive male is less than 4%. These data indicate that even though sexual contact is important in the transmission of STLV-I, it may not be an efficient mode of viral infection. These data also suggest that female-to-male transmission of STLV-I occurs, as recently reported for human T-lymphotropic virus type-I (HTLV-I) infection. These results are important because HTLV-I and STLV-I share many features in common including routes of viral transmission. In addition, the difficulty of clearly quantitating the risk of sexual transmission in humans makes the primate animal model a valuable alternative to study the human infection.

Animals↗
PubMed1993

Cellular localization of CD4 in the human placenta. Implications for maternal-to-fetal transmission of HIV.

CD4 is a 55-kDa glycoprotein that serves as an important cellular differentiation Ag and cell signaling protein on T lymphocytes, as well as a principal receptor for HIV-1 on a variety of cell types including lymphocytes. CD4 receptor expression in syncytiotrophoblasts, the principal cellular barrier in the human placenta, has not been clearly defined. Knowledge concerning the expression of the CD4 receptor on placental trophoblasts is important to define potential mechanisms of transmission of the virus between maternal blood and fetal tissues. Both mature and immature placenta (n = 10) were examined using an avidin D-based immunohistochemical procedure that permits clear morphologic distinction of cell types in placental sections. Syncytiotrophoblasts were defined using anti-cytokeratin mAb (AE1/3), whereas endothelial cells in placental villi were distinctly identified using a mAb directed to CD31. Placental Hofbauer cells (macrophages) and other leukocytes were identified by mAb staining of leukocyte common Ag (CD45). CD4 expression (identified by staining with three separate anti-CD4 mAb) was exclusively localized using this immunohistochemical method to leukocytes in placental villi (e.g., Hofbauer cells); however, no CD4 staining was evident in syncytiotrophoblasts, cytotrophoblasts, or villus endothelial cells. Furthermore, immunoaffinity-purified trophoblasts were negative for CD4 receptor expression. CD4 RNA was not identified in purified trophoblasts using both Northern blot assay and a sensitive polymerase chain reaction method to identify CD4 RNA. In addition, time course studies of purified trophoblasts immediately after purification and at 24, 48, and 72 h in culture indicated that CD4 RNA was not present as a transient, but labile transcript in trophoblasts. These data indicate that the transmission of HIV-1 across syncytiotrophoblasts may occur by mechanisms other than by binding the CD4 receptor and that tissue leukocytes (in particular Hofbauer cells) are likely the principal CD4+ cellular target of HIV-1 in the placenta.

Base Sequence↗
PubMed1993

Atypical human T-cell lymphotropic virus type-I-associated T-cell lymphoma in a low-prevalence Alaska Native population. Implications for disease surveillance.

An atypical case of adult T-cell leukemia/lymphoma (ATL) associated with human T-cell lymphotropic virus type I (HTLV-I) occurred in a 46-year-old Inupiat Eskimo man with no behavioral risk factors for HTLV-I infection. The case was characterized by lack of atypical circulating lymphocytes, hypercalcemia, and opportunistic infections; and by complete remission of the initial renal parenchymal lymphoma. The lymphoma cells had a helper T-cell (CD4) immunophenotype. Serum antibodies to HTLV I/II, detected by Western immunoblot, were identified in specimens collected 31 months before the onset of illness, at the time of diagnosis, and up to 37 months later, shortly before the patient's death. Polymerase chain reaction was used to identify HTLV-I DNA in peripheral blood mononuclear cells and in lymphoma in involved skin. Clinicians should be alert to sporadic cases of both atypical and classic ATL, even in populations in which the prevalence of HTLV-I infection is low.

Alaska↗
PubMed1993

Detection of simian immunodeficiency virus and human immunodeficiency virus type 2 capsid antigens by a monoclonal antibody-based antigen capture assay.

We have tested the ability of a monoclonal antibody-based simian immunodeficiency virus (SIV) p27 capsid antigen assay to detect SIV antigen in supernatants from a variety of infected cell cultures. The antigen capture assay has a sensitivity of approximately 30 pg of SIV p27 capsid antigen/ml. The assay detected SIV p27 capsid antigen in cell culture supernatants from all six strains tested, detected the replication of SIV following the inoculation of the virus in peripheral blood mononuclear cell cultures earlier compared to reverse transcriptase assay, and was more sensitive in detection of the SIV antigen compared to human immunodeficiency virus type 1 (HIV-1) antigen capture assays. The SIV antigen capture assay was used to detect SIV antigen from serum samples and tissue cultures from eight of eight SIVB670-infected rhesus macaques (Macaca mulatta). Similar samples from four control rhesus macaques were negative when tested by the assay. The SIV antigen was detected in virus-infected monkeys during early time periods following inoculation (1 to 3 weeks) or during episodes of CD4+ lymphocytopenia and clinically evident disease. In addition, the SIV antigen capture assay positively identified each of three different HIV-2 strains in cell culture supernatants. The SIV antigen capture assay provides a sensitive and specific method to monitor SIV and HIV-2 capsid antigen in cell cultures and from infected animals. The assay will be an important tool in the utilization of SIV and HIV-2 primate models for HIV-induced acquired immunodeficiency disease syndrome.

Animals↗
PubMed1993

Pathogenesis of lymphoid interstitial pneumonia in natural and experimental ovine lentivirus infection.

Ovine lentivirus (OvLV), as a member of the lentivirinae subfamily of Retroviridae, shares morphological, genomic, and cytopathic features with human immunodeficiency virus (HIV). Although OvLV infection does not induce profound immune deficiency in sheep, it has many similarities with HIV infection, such as the capacity to infect macrophages, undergo antigenic variation in vivo, and induce slow progressive diseases involving the pulmonary, lymphoid, and central nervous systems. Studies of the pathogenesis of disease in sheep naturally or experimentally infected by OvLV are providing clues to the pathogenesis of HIV infection, including the significance of viral load, the emergence of cytopathic variants, the mechanisms and significance of viral antigenic variation, and viral neutralization, and mechanisms of lymphoproliferation and tissue destruction induced by the virus. Preliminary evidence suggests that infection by other microbial agents, including Mycoplasma species, may play a cofactor role in the pathogenesis of lentivirus-associated lymphoid interstitial pneumonia in sheep, but further studies are required to address this issue.

Animals↗
PubMed1992

Characterization of a B-cell immunodominant epitope of human T-lymphotropic virus type 1 (HTLV-I) envelope gp46.

The immune response elicited by a synthetic peptide derived from an immunodominant external envelope region (Env-5, amino acids 242-257) of human T-lymphotropic virus type 1 (HTLV-I) was tested in a rabbit model of HTLV-I infection. The synthetic peptide elicited a strong antibody response to the HTLV-I envelope protein gp46; however, these antibodies failed to inhibit HTLV-I-mediated cell fusion. Immunized rabbits were not protected from HTLV-I infection as determined by seroconversion to viral core proteins by immunoblot, HTLV-I p24 antigen detection in lymphocyte cultures and polymerase chain reaction for the HTLV-I provirus in lymphocyte DNA. Env-5 peptide immunization failed to induce T-cell lymphocyte proliferative responses in rabbits, but induced antibody responses in T-cell deficient Balb c nu/nu mice suggesting that the antigenic determinant represented by the Env-5 peptide is primarily a B-cell epitope. These results further define an immunodominant epitope of the HTLV-I envelope protein and suggest that potential synthetic peptide vaccines against HTLV-I infection must contain multiple antigens that induce both humoral and cellular immune reactivity.

Animals↗
PubMed1992

Simian immunodeficiency virus needlestick accident in a laboratory worker.

The macaque monkey infected with simian immunodeficiency virus (SIV) is an animal model of the acquired immunodeficiency syndrome. We investigated a laboratory worker who was exposed by needlestick accident to blood from an SIV-infected macaque. Seroreactivity to SIV developed within 3 months of exposure, with antibody titres peaking from the third to the fifth month and declining thereafter. Polymerase chain reaction for SIV sequences and cultures of peripheral-blood mononuclear cells failed to show infection. Inoculation of an SIV-negative monkey with blood from the worker did not cause infection. Animal-care and laboratory workers should adhere strictly to recommended procedures to avoid accidental exposures when working with SIV-infected animals or specimens.

Animals↗
PubMed1992

Detection of simian T-lymphotropic virus type I using the polymerase chain reaction.

To develop the polymerase chain reaction (PCR) for the detection of simian T-lymphotropic virus type I (STLV-I) infection, cell lines or peripheral-blood mononuclear cells (PBMC) from 2 non-human primate species [African green monkeys (AGM), Cercopithecus aethiops; baboon, Papio cynocephalus] were evaluated for their STLV-I status using oligonucleotide primer pairs and probes specific for the tax and pol gene regions of the closely related human T-lymphotropic virus type I (HTLV-I). These PCR results were compared with serologic (Western blot assay) and viral culture (p24-antigen capture assay) data. PCR products for both gene regions were detected in established baboon, Japanese macaque and rhesus macaque STLV-I-producing cell lines. STLV-I tax and pol products were also detected in PBMC from 4 of 4 infected AGM and 4 of 4 infected baboons, each of which were also Western-blot-positive and p24-antigen-capture-positive. Of the remaining AGM (n = 7) and baboon (n = 1) which were PCR-negative, each was also Western-blot-negative and p24-antigen-capture-negative. Two seronegative and virus-culture-negative AGM were classified as PCR indeterminate with weak reactivity using tax primers. These primer pairs failed to amplify DNA from uninfected human PBMC, an uninfected human lymphoid cell line, a simian immunodeficiency virus macaque (SIVmac251)-infected cell line and a simian-retrovirus-type-D(SRV-D)-infected cell line. HTLV-II-pol-specific primer pairs failed to amplify DNA from STLV-I-infected cell lines and PBMC from STLV-I-infected monkeys. Further, HTLV-I pol and tax primer pairs successfully amplified RNA from HTLV-I- and STLV-I-infected cell lines by reverse transcriptase (RT)-PCR. We have demonstrated excellent specificity in the detection of STLV-I by PCR using these HTLV-I-derived primers and probes. Additionally, our data suggest that the tax and pol gene regions are conserved between HTLV-I and STLV-I strains found among these diverse species of non-human primates.

Animals↗
PubMed1992

Comparative biological responses of rabbits infected with human T-lymphotropic virus type I isolates from patients with lymphoproliferative and neurodegenerative disease.

An experimental rabbit model was used to determine host responses to infection by various human T-lymphotropic virus type-I (HTLV-I) strains. Seven groups of 4 to 5 rabbits each were inoculated with lethally-irradiated HTLV-I-infected cell lines derived from patients with adult T-cell leukemia/lymphoma or from patients with HTLV-I-associated myelopathy. Four separate control groups of 2 rabbits each were inoculated with similarly prepared HTLV-I-negative cells derived from rabbits or humans. Anti-viral antibody responses were assessed by immunoblot assay and hematologic parameters were measured using automated cell counters and cytologic staining. The virologic status of challenged rabbits was determined by co-culture and HTLV-I antigen capture assay, as well as by polymerase chain reaction (PCR) amplification of HTLV-I DNA from peripheral blood mononuclear cells (PBMC) or tissues. The HTLV-I inocula could be separated into groups based upon their infectivity to rabbits: highly infectious strains elicited intense serologic responses and were detected frequently in tissues by antigen and PCR assays, while other strains were moderately to poorly infectious, induced weak antibody responses and were infrequently detected by antigen and PCR assays. Overall, PBMC appeared to have the greatest quantity of HTLV-I containing cells, while bone marrow was a poor source of virus. No clinical or hematologic abnormalities were evident during the 24-week course of infection. Taken together, our results suggest there is heterogeneity in the biological response to HTLV-I infection which is, in part, dependent on the infecting strain of virus.

Animals↗
PubMed1992

Concomitant augmentation of CD4+ CD29+ helper inducer and diminution of CD4+ CD45RA+ suppressor inducer subset in patients infected with human T cell lymphotropic virus types I or II.

To examine the immunomodulatory effects of HTLV infection, lymphocyte subset analysis was performed on patients infected with human T cell lymphotropic virus type-I (HTLV-I, n = 6) or -II (HTLV-II, n = 12) and on normal blood donors (n = 16). The percentages of total B lymphocytes (CD19), natural killer (NK) cells (CD16), T lymphocytes and their subsets (CD2, CD3, CD4, CD5, CD7, CD8), and IL-2R (CD25) were found to be within the range found in normal donors. However, the expression of CD8+ HLA-DR+ increased significantly in patients with HTLV-I or HTLV-II infection (14.1 +/- 3.9% and 9.7 +/- 2.4% respectively; P less than 0.01) when compared with controls (3.2 +/- 1.1%). In addition, there was a significantly greater proportion of CD4+CD29+ T lymphocytes (29.3 +/- 6.1% and 31.1 +/- 9.0%; P less than 0.05) with concomitant diminution of CD4+CD45RA+ T lymphocytes (8.3 +/- 3.3% and 11.4 +/- 1.5%; P less than 0.01) in patients infected with HTLV-I or HTLV-II respectively, when compared with controls. The increased percentage of CD4+CD29+ subpopulations showed a direct correlation (rs = 0.86; P less than 0.001) with HTLV-specific antibody production. No difference in the CD8 population coexpressing CD29 and S6F1 (an epitope of LFA-1) were observed in the HTLV-infected group when compared with normal donors and functional analysis exhibited minimal cytotoxicity against lectin labelled heterologous target cells. Thus, the shift in the suppressor/cytotoxic to helper/inducer 'memory' CD4+ may be associated with immunoregulatory abnormalities often found in persons infected with HTLV-I or HTLV-II.

Antigens, CD↗
PubMed1992

Serologic confirmation of simian T-lymphotropic virus type I infection by using immunoassays developed for human T-lymphotropic virus antibody detection.

Serum specimens from diverse species of Old World monkeys, categorized as seropositive (n = 97) or seronegative (n = 23) for human T-lymphotropic virus (HTLV) infection, were tested by using recombinant env-spiked Western immunoblot assays and synthetic peptide assays for simultaneous detection and discrimination of simian T-lymphotropic virus (STLV) infection. Of the 97 seropositive specimens, 93 reacted with the recombinant transmembrane (r21env) protein and 90 reacted with a recombinant, MTA-1, derived from the central region of the external glycoprotein of HTLV-I (rgp46env), thus yielding test sensitivities of 96 and 93%, respectively. While 1 of the 23 negative monkey specimens reacted with r21env, none reacted with rgp46env, for overall specificities of 96 and 100%, respectively. Analysis of synthetic peptide-based immunoassays demonstrated that while 85 of 97 (88%) seropositive specimens reacted with HTLV-I-specific epitope (p19gag), none of the specimens reacted with HTLV-II-specific epitope (gp52env). These results show that recombinant envelope-spiked Western blots provide a simple means for serologic confirmation of STLV-I infection and that type-specific synthetic peptides can be used to confirm the virus type in seropositive monkey specimens.

Animals↗
PubMed1991

Constitutive expression of c-jun and jun-B in cell lines infected with human T-lymphotropic virus types I and II.

To better understand the transcriptional regulation of human T-lymphotropic viruses, expression of the nuclear proto-oncogenes, jun-B and c-jun were examined in cell lines infected with HTLV-I/II. Constitutive high levels of jun-B and c-jun expression were observed in HTLV-I (MT-2, Hut-102, IR, FS, SP) and HTLV-II infected cell lines (Mo-T, PAN). In contrast, the uninfected cell lines (Jurkat, Hut-78) expressed only basal levels of jun. This expression of jun was not dependent upon IL-2, as both IL-2 dependent (IR, FS, SP, and Pan) and IL-2 independent (MT-2, Hut-102, Mo-T) cell lines constitutively expressed transcripts for jun-B and c-jun. These data demonstrate that deregulated expression of nuclear protooncogenes such as jun may lead to cellular proliferation and the protein products of these nuclear oncogenes may potentially serve as transcriptional activators of HTLV-LTR by complexing with other nuclear proteins.

Blotting, Northern↗
PubMed1991

Infectious transmission of human T-cell lymphotropic virus type II in rabbits.

To determine the susceptibility of rabbits to experimental infection with human T-cell lymphotropic virus type-II (HTLV-II), four separate groups of four weanling rabbits each were inoculated intravenously with lethally irradiated HTLV-II-infected human cell lines Mo-T (HTLV-IIMo-infected T cells), WIL-NRA (an Epstein-Barr virus [EBV]-transformed B-lymphoblastoid cell line infected with HTLV-IINRA), 729pH6neo (an EBV-transformed lymphoblastoid cell line transfected with a molecular clone of HTLV-IIMo), or G12.1 (HTLV-II-infected T cells from a Panamanian Guaymi Indian). Two additional groups of four rabbits each were similarly inoculated with control uninfected 729 or HuT 78 cells. Early and persistent seroconversion to HTLV-II core antigen p24, as determined by Western immunoblot, occurred in all HTLV-II-inoculated rabbits and was most intense in rabbits inoculated with G12.1 cells; seroreactivity to other HTLV-II gag or env antigens occurred later, with less intensity, or not in all inoculated rabbits. Peripheral blood mononuclear cells (PBMC) and other lymphoid cells from HTLV-II-inoculated rabbits produced minimal p24 in vitro, as determined by enzyme immunosorbent capture assay. Virus was more readily detected by polymerase chain reaction amplification of HTLV-II pol sequences; this occurred most frequently in rabbits inoculated with Mo-T cells, and most frequently in PBMC as compared with other tissues tested (bone marrow, brain, and liver). No evidence of disease occurred in HTLV-II-inoculated rabbits observed for as long as 24 weeks. All control rabbits remained negative for evidence of HTLV-II infection, as determined by the same procedures. These results provide the first evidence of HTLV-II infection in a species other than humans, and demonstrate the usefulness of the rabbit as an animal model to study the biologic response to different isolates of this human retrovirus.

Animals↗