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Biomedical subjects

R C Gallo

Publications and source records attributed to R C Gallo.

At least 361 records · Page 20Linked to original sources
PubMed1986

Pathogenesis of B cell lymphoma in a patient with AIDS.

Lymphoma occurs at increased frequency in patients with the acquired immunodeficiency syndrome (AIDS). We studied, using serologic and molecular techniques, one such lymphoma for (a) evidence of infection with human T lymphotropic virus, type III (HTLV-III), and Epstein-Barr virus (EBV), (b) monoclonal rearrangement of immunoglobulin and T cell receptor genes, and (c) rearrangement of the c-myc oncogene. Immunoglobulin and T cell receptor gene studies demonstrated that the tumor was of monoclonal B cell origin. Similar to cases of Burkitt's lymphoma unrelated to AIDS, there were DNA sequences in the lymphoma that hybridized to EBV-specific probes and demonstrated evidence of c-myc rearrangement. HTLV-III sequences were not detected in the malignant B cells. The pathogenesis of some B cell neoplasms in patients with the syndrome may involve transformation by EBV and deregulation of oncogene expression without direct infection of the malignant B cells by HTLV-III.

Acquired Immunodeficiency Syndrome↗
PubMed1986

Human T lymphotropic virus type III infection of human alveolar macrophages.

The human T-cell lymphotropic virus type III (HTLV-III) is the etiologic agent of the acquired immunodeficiency syndrome (AIDS) and preferentially infects T4 lymphocytes. Other cell types, notably B lymphocytes and other nonlymphoid cells, also have been reported to be infected in vitro by HTLV-III. We now report on the susceptibility of human pulmonary macrophages to infection with HTLV-III in vitro. Alveolar macrophages infected with HTLV-III produced low levels of virus that could be transferred to allogeneic human peripheral blood mononuclear leukocytes as long as 2 weeks after initiation of infection. Unlike HTLV-III infection of T lymphocytes, macrophages appeared more resistant to viral-mediated cytopathic effects. Primary cultures of pulmonary macrophages from two of four patients with AIDS spontaneously produced low levels of virus detected as precipitable reverse transcriptase activity, suggesting that these cells were infected in vivo. Because tissue macrophages are long-lived cells, they may act as a reservoir of HTLV-III, capable of transmitting the virus to other susceptible cells such as T lymphocytes, causing periodic low-level viremia. Macrophage infection with HTLV-III may be one mechanism for the establishment of viral persistence in infected hosts.

Acquired Immunodeficiency Syndrome↗
PubMed1986

AIDS pandemic.

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Acquired Immunodeficiency Syndrome↗
PubMed1986

HTLV-III expression in infected lymph nodes and relevance to pathogenesis of lymphadenopathy.

In situ hybridization with a 35S-labeled probe of cryosections from 14 lymph nodes of HTLV-III/LAV-seropositive individuals with lymphadenopathy showed the presence of rare cells containing HTLV-III RNA at levels consistent with virus replication. Positive cells were observed at a frequency of only 1-10 per section. In all lymph nodes studied, including those showing follicular hyperplasia or involution, most of the cells expressing viral RNA were present in the follicular areas. Only a minority of such cells were found outside the follicles. The nature of the follicular, virus-replicating cells was not evident from the processed cryosections. After prolonged autoradiography, another pattern of hybridization was observed, suggesting low levels of viral RNA diffusely distributed throughout most, but not all, follicles. This may represent extracellular virus and/or virus-antibody complexes, but was not consistent with intracellular viral RNA or phagocytosed virus particles. Comparison of hybridization levels in relation to histology suggested a decrease in both the number of HTLV-III replicating cells as well as in the diffusely distributed viral RNA with progression of follicular involution. Our observations indicate that in HTLV-III-infected subjects, lymph node follicles are an important site of virus replication and trapping, suggesting a decisive role of the virus in the characteristic reactive and cytopathogenic changes of HTLV-III-associated lymphadenopathy.

AIDS-Related Complex↗
PubMed1985

Prevalence of HTLV-I in Arctic regions.

Sera of native inhabitants of Arctic regions were assayed for antibodies to HTLV-I by the ELISA technique followed by competition experiments to confirm antibody specificity. Residents of 7 widely separated Alaskan villages exhibited prevalence rates of 0 to 12% for HTLV-I antibodies. Less than 1% of Greenland Eskimos were HTLV-I antibody-positive. Residents of 3 northern Swedish regions ranged in HTLV-I antibody prevalence from 0 to 5%. Sera of healthy native inhabitants of Alaska and northern Sweden were similarly assayed for antibodies to HTLV-II. No additional sera were shown to be positive for HTLV-II antibodies. While some of the HTLV-I antibody-positive sera exhibited cross-reactivity with HTLV-II antigens, competition experiments using disrupted HTLV-II or purified HTLV-I p24 as test antigens indicated that the primary antibody response in all cases tested was elicited by HTLV-I. Our results show that HTLV-I distribution is not restricted to endemic areas in warm, humid climates, but extends to Arctic regions. Within these regions, HTLV-I exhibits the same restricted distribution seen in other areas where virus infection is prevalent. The Arctic does not seem to be a reservoir for HTLV-II infection. The origin of HTLV-I in Arctic areas is not known. One may speculate that foreign visitors introduced the virus into Aleut and Lapp populations, and that it has been maintained there and restricted in its distribution as a result of close familial relationships.

Adolescent↗
PubMed1985

Seroepidemiological studies of HTLV-III antibody prevalence among selected groups of heterosexual Africans.

T-lymphocyte subsets and human T-cell lymphotropic virus type III antibody prevalence were studied in African patients with the acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC), and in female prostitutes. African blood donors and healthy Zairian and Rwandese persons matched for age, sex, and annual income served as controls. Seropositivity was noted in 46 (87%) of 53 patients with AIDS, 29 (88%) of 33 patients with ARC, 67 (80%) of 84 prostitutes, and five (12.5%) of 40 and eight (15.5%) of 51 healthy controls and blood donors, respectively. Patients with AIDS and ARC had a significantly lower OKT4/OKT8 ratio than healthy African controls. These studies suggest that human T-cell lymphotropic virus type III infection has already spread extensively into the general African population and that female prostitutes could be an important human reservoir of AIDS virus in the heterosexual population.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Heterosexually acquired HTLV-III/LAV disease (AIDS-related complex and AIDS). Epidemiologic evidence for female-to-male transmission.

Thirty-seven percent (15/41) of patients with human T-cell lymphotropic virus type III (HTLV-III) disease (acquired immunodeficiency syndrome [AIDS] or AIDS-related complex) sequentially evaluated at Walter Reed Army Medical Center, Washington, DC, acquired this infection from a partner(s) of the opposite sex. Demographic features of these 15 patients (ten males and five females) differed substantially from those for patients reported to the Centers for Disease Control. Heterosexual contact with partners who developed AIDS or who were at risk for AIDS was confirmed in six patients. The remaining nine patients had multiple (greater than 50) heterosexual partners and/or sexual contact with prostitutes. The method of sexual activity did not appear to be related to disease acquisition; however, this study clearly demonstrated that receptive anal intercourse was not a requirement. The observations reported herein provide further epidemiologic evidence to support the occurrence of bidirectional heterosexual transmission (both male to female and female to male) of HTLV-III infection and disease.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Human T-cell leukemia/lymphotropic virus type III in the conjunctival epithelium of a patient with AIDS.

The human T-cell leukemia/lymphotropic virus type III (HTLV-III), the causative agent of the acquired immunodeficiency syndrome (AIDS), has been isolated from the conjunctival epithelium of a 33-year-old woman with AIDS, suggesting that an important reservoir of the virus may be the ocular surface epithelial cells. The tears and conjunctival epithelium from normal controls were negative for HTLV-III. The finding of HTLV-III in the tears and conjunctival epithelium indicated that HTLV-III may be ubiquitous in bodily cells and fluids. Repeated contact with the tears and ocular surface epithelium of patients with AIDS may possibly facilitate transmission of HTLV-III, and precautions are advisable during routine ophthalmologic procedures such as glaucoma testing and contact-lens fitting.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Characterization of gp41 as the transmembrane protein coded by the HTLV-III/LAV envelope gene.

Radiolabeled amino acid sequencing was used to characterize gp41, an antigen of HTLV-III/LAV, the virus believed to be the etiological agent of the acquired immune deficiency syndrome. This antigen is the one most commonly detected in immunoblot assays by sera of patients with AIDS or AIDS-related complex (ARC) and other individuals infected with HTLV-III/LAV. A mouse monoclonal antibody that was reactive with gp41 precipitated a 160-kilodalton protein (gp160) in addition to gp41, but did not precipitate a 120-kilodalton protein (gp120) from extracts of metabolically labeled cells producing HTLV-III. Extracts of infected cells that had been labeled with tritiated leucine or isoleucine were immunoprecipitated with the monoclonal antibody. The immunoprecipitates were fractionated by polyacrylamide gel electrophoresis and the p41 was eluted from the gel bands and subjected to amino-terminal radiolabeled amino acid sequencing by the semiautomated Edman degradation. Leucine residues occurred in cycles 7, 9, 12, 26, 33, and 34 among 40 cycles and isoleucine occurred in cycle 4 among 24 cycles analyzed. Comparison of the data with the deduced amino acid sequence of the env gene product of HTLV-III precisely placed gp41 in the COOH-terminal region of the env gene product. Gp160 is thus the primary env gene product and it is processed into gp120 and gp41.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Female prostitutes: a risk group for infection with human T-cell lymphotropic virus type III.

In July, 1984 33 female prostitutes in Rwanda and 25 male customers of prostitutes were assessed clinically and for their T-lymphocyte subsets and frequency of antibodies to human T-cell lymphotropic virus type III (HTLV-III). 27 healthy males who denied contact with prostitutes, 33 healthy women who were not prostitutes, and 51 Rwandese prostitutes seen in 1983 served as controls. Only 6 prostitutes were symptom-free (group I), 13 had unexplained generalised lymphadenopathy (LAP) (group II), and 14 had LAP and constitutional symptoms (group III). Mean OKT4/OKT8 ratio in groups II and III was significantly lower than that in group I or in female controls. HTLV-III antibodies were detected in 29 of 33 prostitutes, 4 female controls, 7 male customers, and 2 male controls. In male customers, HTLV-III seropositivity increased according to the number of different sexual partners per year. This study suggests that in Central Africa prostitutes are a high-risk group for HTLV-III infection.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Isolation of human T-lymphotropic virus type III from the tears of a patient with the acquired immunodeficiency syndrome.

Human T-lymphotropic virus type III (HTLV-III) was isolated from the tears of 1 out of 7 patients with the acquired immunodeficiency syndrome (AIDS) or the AIDS-related complex. The tears from 5 healthy individuals did not show HTLV-III. The recovery of HTLV-III from tears suggests that they may harbour free virus or contain virus-positive cells and is consistent with the recovery of HTLV-III from other body fluids. Although casual contact with such fluids has not been shown to cause AIDS, direct contact with the tears of AIDS patients, including contact during routine ophthalmologic procedures, should be minimised.

Acquired Immunodeficiency Syndrome↗