Suppression of delayed-type hypersensitivity to PPD and PHA in elderly HTLV-I carriers

Article Abstract:

The immune system of patients who are infected with human T-cell leukemia virus type I (HTLV-I) and have developed adult T-cell leukemia (ATL) is suppressed. However, the status of the immune system in carriers of HTLV-I, who are healthy and have no disease symptoms, is not certain. Previous studies have shown that the immune reaction to the tuberculin skin test, which measures delayed-type hypersensitivity (DTH), is suppressed in HTLV-I carriers in Japan, where HTLV-I infection is endemic. The suppression is more pronounced in individuals who are elderly, aged 60 years or older. Other types of DTH, reaction to purified protein derivative (PPD) of tuberculin and phytohemagglutinin (PHA), were examined in 56 patients, aged from 62 to 93 years old. The subjects were hospitalized with diseases that did not cause a suppression of the immune system. Twenty-two (39 percent) had antibodies to HTLV-I, indicating infection, but none had symptoms of disease caused by HTLV. There was an increased level of nonreactivity to PPD and PHA with increasing age. The degree of nonreactivity was greater in carriers than in non-carriers. Eighty-eight percent (15 out of 17) of HTLV-I carriers were nonreactive to both antigens, compared with 60 percent (15 out of 25) of non-carriers. Among the carriers who reacted to the antigens, the degree of reaction to PPD was reduced, but reaction to PHA was not reduced. These results confirm the finding that older individuals who are carriers of HTLV-I have reduced DTH response. (Consumer Summary produced by Reliance Medical Information, Inc.)

Aging, Analysis, Causes of, Demographic aspects, Immunosuppression, HTLV infections, Delayed hypersensitivity, Virus-induced immunosuppression

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High incidence of antibodies to HTLV-I tax in blood relatives of adult T cell leukemia patients

Article Abstract:

Adult T cell leukemia (ATL; uncontrolled growth of white blood cells) is caused by the human T cell leukemia virus (HTLV-I). It is not clear how the virus causes this disease. While HTLV-I is found in all ATL cells, it does not cause disease in all individuals it infects; instead, most remain healthy carriers of the HTLV-I virus. Why only some individuals progress to ATL or other associated diseases is unknown. There is evidence of a higher rate of HTLV-I in family members of ATL patients, suggesting transmission of the infection within the family or an effect of genetic backgrounds shared by blood relatives. Research has shown that a gene called the tax gene may potentially induce leukemia. Based on the assumption that this is true, and that ATL frequently occurs in families, a study was developed to test the prevalence of tax proteins (by testing for antibodies to tax proteins) in HTLV-I infected people, compared with matched (for age) HTLV-I-positive blood donors. It was found that direct offspring of ATL patients produced more antibodies than their HTLV-I-positive blood donor matches. This suggests possible differences in time or route of transmission of HTLV-I infection, or differences in the strain of virus within families, compared with strains among non-blood-relatives. (Consumer Summary produced by Reliance Medical Information, Inc.)

Development and progression, Genetic aspects, Disease transmission, Leukemia, Viral antibodies, HTLV-I (Virus)

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Increased expression of interleukin-2 receptor alpha on peripheral blood mononuclear cells in HTLV-I tax/rex mRNA-positive asymptomatic carriers

Article Abstract:

The tax gene of human T-cell lymphotropic virus type I (HTLV-I) may be responsible for the proliferation of T cells that results in adult T-cell leukemia. Blood samples were taken from 194 HTLV-I carriers and classified into four groups depending on whether HTLV-I proviral DNA levels were high, medium, low or undetectable. The polymerase chain reaction detected tax RNA in 3% of the samples with low or undetectable levels but in 40% of the samples with high levels. Blood samples with high proviral DNA levels also had a greater percentage of cells with the interleukin-2 receptor, which can cause cell proliferation.

Measurement, HTLV-I infections, Messenger RNA, Interleukin-2, Drug receptors

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