Pamela Rodgers‐Johnson

HTLV-1 and polymyositis in Jamaica

IgG antibodies to human T-cell lymphotropic virus (HTLV-1) were found in 11 of 13 (85%) Jamaican patients with idiopathic adult polymyositis. The association was first observed in 7 patients with polymyositis who were included in a control group of 100 patients with neurological and neuromuscular diseases in a serological investigation of the prevalence of HTLV-1 antibody in patients with tropical spastic paraparesis. All 7 patients with polymyositis were positive for the antibody by an enzyme-linked immunosorbent assay, confirmed by western blot. Because of this striking association a further 6 patients with polymyositis were identified and tested, 4 of whom were also seropositive for HTLV-1 antibody.

INFECTION OF CHIMPANZEES BY HUMAN T-LYMPHOTROPIC RETROVIRUSES IN BRAIN AND OTHER TISSUES FROM AIDS PATIENTS

The authors report the isolation of acquired immunodeficiency syndrome (AIDS) associated retroviruses from packed leukocytes of 2 chimpanzees inoculated intracerebrally and intravenously with brain tissue suspension from 2 patients with AIDS encephalopathy on days 7 and 14 after inoculation. Antibody to the AIDS-associated retroviruses has appeared in sera of 2 chimpanzees inoculated intravenously with plasma from different AIDS patients in 1 chimpanzee inoculated intravenously with brain and thymus suspension and in 1 chimpanzee inoculated intracerebrally with brain tissue suspension from a patient with AIDS encephalopathy. 11 chimpanzees inoculated with supernatant fluids from tissue cultures infected with human T-lymphotropic virus type III (HTLV-III) lymphadenopathy-associated virus (LAV) and IDAV have acquired antibodies to the LAV/HTLV-III viral antigens 2-8 weeks after inoculation. Virus was recovered from the lymphocytes of all 6 seroconverted animals between 8-154 days after primary inoculation of HTLV-III. 2 animals have severe suppression of T-cell function. However all 23 chimpanzees that have seroconverted to HTLV-III or LAV antigen have remained clinically well for 2-15 months of follow-up. There have been no tumors lymphadenopathy or severe opportunistuc infections. Other species of non-human primates similarly inoculated with HTLV-III and LAV have not seroconverted 2-10 months postinoculation. These findings confirm the active and persistent virus infection of chimpanzees with retroviruses derived from AIDS patients. They further establish the presence of viruses in the plasma and brain of AIDS patients by direct transmission of their virus to chimpanzees.

Incidence of HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) in Jamaica and Trinidad

HTLV-I is sexually transmitted more efficiently from men to women than vice versa, and the majority of HTLV-I endemic areas report a female preponderance of HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) cases. The objective of this study was to estimate the gender- and age-specific incidence rates of HAM/TSP in the general population as well as in the HTLV-I-infected population in Jamaica and in Trinidad and Tobago. Incidence rates for HAM/TSP were computed based on all reported incident cases in both countries between 1990 and 1994. Population census reports for 1990 were used to calculate the population at risk. The age-standardized HAM/TSP incidence rate (mean +/- standard error of the mean) in Jamaica was 1.8 +/- 0.2/100,000 person years (PY). Among individuals of African descent in Trinidad and Tobago, the rate was 1.7 +/- 0.4/100,000 PY. As in HTLV-I seroprevalence, the incidence rate of HAM/TSP increased with age through the fifth decade of life and was three times as high in women than in men. The HAM/TSP incidence rate, calculated as a function of the number of HTLV-I-infected persons in each age stratum, is higher in women (24.7/100,000 PY) than in men (17.3/100,000 PY). With HTLV-I infection, the lifetime risk of developing HAM/TSP was estimated to be 1.9% overall and is slightly higher in women (1.8%) than in men (1.3%). Thus, the higher prevalence of HTLV-I in women in endemic areas does not fully explain the preponderance of female HAM/TSP, suggesting that other cofactors must be present. The higher incidence rate in women between the ages of 40 and 59 years, as well as the increase in HAM/TSP incidence rates with age, are indicative of the importance of adult-acquired HTLV-I infection, presumably through sexual transmission.

Tropical myeloneuropathies--a new aetiology.

Abstract Tropical myeloneuropathies are a group of neurological disorders known to occur in subtropical and tropical regions. Many aetiologies have been postulated and investigated over the past 100 years, but no single cause has been found. Recent studies suggest that human T-cell lymphotropic virus HTLV-I is the causative agent of one of these tropical myeloneuropathies, endemic tropical spastic paraparesis, and of a related disorder in southern Japan called HTLV-I-associated myelopathy. Endemic tropical spastic paraparesis is now being reported from geographical and climatic regions that were previously thought to be free of these disorders.

High prevalence of human T-lymphotropic virus type I infection in isolated populations of the Western Pacific region confirmed by Western immunoblot

High prevalences of antibodies against human T‐lymphotropic virus type I (HTLV‐I), as confirmed by Western immunoblot, were found in several remote indigenous populations of the Solomon Islands and Vanuatu and in some isolated populations of New Guinea that had no contact with Japanese or Africans and little contact with Caucasians prior to our bleedings. By contrast, zero or very low prevalences of HTLV‐I infection were found in Guamanians and Carolinians, despite more than 30 years of intense contact with the Japanese. A total of 1,601 sera, collected between 1963 and 1981 from 21 population groups in the Western Pacific, was tested by enzyme‐linked immunosorbent assay (ELISA) for IgG antibodies to HTLV‐I. By ELISA, prevalences of antibodies against HTLV‐I ranged from zero to 50%. Seropositivity could be confirmed in only 12.5% of 48 ELISA‐positive sera selected for testing by Western immunoblot. However, the confirmed HTLV‐I seroprevalences in some Melanesian populations were still as high as those found in HTLV‐I‐endemic regions, such as southwestern Japan and the Caribbean basin. HTLV‐I prevalences were similar among males and females, and acquisition of antibodies increased with age. Our data indicate that infections with HTLV‐I or a related retrovirus have been widespread in the southwestern Pacific for over 25 year in populations with minimal outside contact, while some populations which had extensive Japanese contact have no evidence of infection. Furthermore, based on the high frequency of indeterminate Western immunoblots, we conclude that in Melanesia this may represent either incomplete specific reactivity to HTLV‐I or the existence of an antigenic variant of HTLV‐I, distinct from prototype Japanese, American, and European HTLV‐I strains.

Ultrastructural Pathology of Human T-Cell Lymphotropic Virus Type I Encephalomyelopathy in a White Patient with Adult T-Cell Leukemia/Lymphoma

A white patient with human T-cell lymphotropic virus type I (HTLV-I)-associated adult T-cell leukemia/lymphoma for 10 years died 4 months after the onset of spastic myelopathy. Ultrastructurally, the neuropathologic findings consisted of dystrophic neurites (spheroids) filled with neurofilaments or electron-dense bodies, intense astrocytic reaction with abundant formation of corpora amylacea, and multilamellar bodies. Demyelination and spongiform change were absent. Viruslike particles resembling HTLV-I were detected adjacent to brain endothelial cells.

Human T-lymphotropic virus type I: A retrovirus causing chronic myeloneuropathies in tropical and temperate climates

Human T‐cell lymphotropic virus type I (HTLV‐I), the first human retrovirus to be isolated, is the cause of endemic tropical spastic paraparesis (TSP). Originally, this chronic neurological disorder was described as a disease seen among blacks of low socioeconomic status living in tropical countries, and thus for many decades TSP remained a little known curiosity outside the endemic regions. The link between HTLV‐I infection and TSP was made fortuitously, when antibodies to HTLV‐I were found in serum and cerebrospinal fluid of TSP patients in Jamaica, Colombia, and Martinique. Soon thereafter a similar disorder, designated HTLV‐I associated myelopathy (HAM), was reported from southern Japan. This broadened the geographic and ethnic boundaries of this chronic myelopathy and the disease has now been reported in multiple ethnic groups from more than 40 countries, in both tropical and temperate regions. The name TSP/HAM is now used to include all patients (regardless of race or country of origin) who have HTLV‐I‐positive endemic TSP or HAM.