Human T‐lymphotropic virus type 1 (HTLV‐1) is the agent of the HTLV‐1‐associated myelopathy/tropical spastic paraparesis (HAM/TSP), which may occur in >5% of patients during their lifetime. HTLV‐1‐infection causes disturbances in the immune system, and the viral load may also play an important role in the pathogenesis of HAM/TSP. Some cytokines are involved in the pathogenesis of this disorder. We have determined IL‐2, IL‐4, IL‐10, IL‐12 p70, IFN‐γ and TNF‐α production among HTLV‐1‐infected subjects from our HTLV‐out Clinic in Institute of Infectious ‘Emílio Ribas’ in Sao Paulo city, Brazil. PBMC obtained from healthy controls (n = 32), asymptomatic HTLV‐1 carriers (n = 68) and HAM/TSP patients (n = 44) were grown in the absence and in the presence of phytohaemagglutinin (PHA), and the supernatants’ fluids were measured for cytokines production. IL‐2 levels were increased in the asymptomatic HTLV‐1 carriers, and IFN‐γ was increased in both groups of patients (asymptomatic HTLV‐1 carriers and more significantly among HAM/TSP patients). IL‐4, IL‐10, TNF‐α and IL‐12 p70 levels were not significantly increased on both groups of patients, as compared with controls. The major finding of this study is that IFN‐γ was an important cytokine for the HAM/TSP pathogenesis. Therefore, immune modulation of IFN‐γ may be critical to treat of HAM/TSP patients.

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Although many authors have considered ID to be a form of childhood dermatitis, we have described four cases that fulfilled the major criteria for ID, except for onset in adulthood.

Although human T-cell lymphotropic virus type 2 (HTLV-2) is considered of low pathogenicity, serological diagnosis is important for counseling and monitoring. The confirmatory tests most used are Western blot (WB) and PCR. However, in high-risk populations, about 50% of the indeterminate WB were HTLV-2 positives by PCR. The insensitivity of the WB might be due to the use of recombinant proteins of strains that do not circulate in our country. Another possibility may be a high level of immunosuppression, which could lead to low production of virus, resulting in low stimulation of antibody. We found one mutation, proline to serine in the envelope region in the position 184, presented at least 1/3 of the samples, independent the indeterminate WB profile. In conclusion, we found no correlation of immune state, HTLV-2 proviral load, or env diversity in the K55 region and WB indeterminate results. We believe that the only WB kit available in the market is probably more accurate to detect HTLV-1 antibodies, and some improvement for HTLV-2 detection should be done in the future, especially among high-risk population.

The present study evaluated the in vitro response to different mitogens and a candidin antigen (CMA) in Human T‐cell lymphotropic virus type 1 (HTLV‐1) and co‐infected HIV‐1/HTLV‐1 patients, to identify if this co‐infection may modify the spontaneous lymph proliferative response. Peripheral blood mononuclear cells from 72 healthy seronegative controls, 75 asymptomatic HTLV‐1‐infected carriers, 42 HAM/TSP cases, 33 solely HIV‐1‐infected subjects and 24 HIV‐1/HTLV‐1 patients were assayed in the presence and absence of mitogens (PHA, PWM and OKT3) and CMA. The HAM/TSP group had the highest proliferation rate at 3 and 6 days after culture. HAM/TSP cases showed decreased response to PHA, compared with asymptomatic HTLV‐1 subjects, and most important, the co‐infected HIV‐1/HTLV‐1 cases presented a similar response to HTLV‐1‐infected subjects after 3 days of culture. The singles HIV‐1‐infected group had decreased in vitro response. It appears that during co‐infection, the HTLV‐1 regulatory proteins overwhelm the action of HIV‐1 regulatory proteins.