Immune reconstitution inflammatory syndromes (IRISs) have been reported in patients with human immunodeficiency virus/acquired immunodeficiency syndrome (AIDS) since the introduction of highly active antiretroviral therapy (HAART). This syndrome is characterized by clinical manifestations of opportunistic infections when signs of immune reconstitution are observed during therapy. We report on leishmaniasis, suggestive of HAART-induced IRIS, in 2 patients with AIDS. After beginning HAART, 1 patient presented with disseminated, tegumentary lesions, whereas the other patient's preexisting lesions worsened and became more extensive; however, at the same time, their CD4(+) T cell counts were recovering and their virus loads were decreasing significantly. The lesions healed with anti-Leishmania therapy.
Clinical manifestations of tegumentary leishmaniasis in HIV-infected patients are diverse. Our data emphasize possible unusual manifestations of this disease in HIV-infected patients, particularly in severely immunosuppressed cases (< 200 CD4+ cells mm(-3)).
To evaluate the human T-cell lymphotropic virus type I (HTLV-I) proviral DNA load among asymptomatic HTLV-I-infected carriers and patients with HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP), real time PCR using TaqMan probes for the pol gene was performed in two million peripheral blood mononuclear cells (PBMC). The albumin gene was the internal genomic control and MT2 cells were used as positive control. The results are reported as copies/10,000 PBMC, and the detection limit was 10 copies. A total of 89 subjects (44 HAM/TSP and 45 healthy HTLV-I-infected carriers) followed up at the Institute of Infectious Diseases "Emilio Ribas" and in the Neurology Division of Hospital of Clínicas were studied. The asymptomatic HTLV-I-infected carriers had a median number of 271 copies (ranging from 5 to 4756 copies), whereas the HAM/TSP cases presented a median of 679 copies (5-5360 copies) in 10,000 PBMC. Thus, HAM/TSP patients presented a significantly higher HTLV-I proviral DNA load than healthy HTLV-I carriers (P = 0.005, one-way Mann-Whitney test). As observed in other persistent infections, proviral DNA load quantification may be an important tool for monotoring HTLV-I-infected subjects. However, long-term follow-up is necessary to validate this assay in the clinical setting.
Two hundred ninety-three individuals, who were enrolled in the HTLV out-clinic in Sao Paulo city, Brazil, between July 1997 and May 2003, were tested by EIAs, and positive sera 232 (79%) reactive by one of the tests. When these sera were tested by WB revealed 134 were HTLV-I, 28 HTLV-II, 4 HTLV-I/II, and 48 were indeterminate. Polymerase chain reaction (PCR) on the indeterminate group showed that 20 (42%) were HTLV-II and 28 were negative. From a total of 48 HTLV-II subjects with DNA available, restriction fragment length polymorphism (RFLP) of the env region revealed 47 HTLV-IIa and 1 HTLV-IIb. The phylogenetic analysis was performed on 23 samples, which identified 19 as subtype a, Brazilian subcluster, and 4 as subtype b. This is the first time HTLV-II subtype b has been described in Brazil. However, further studies, such as a complete nucleotide DNA sequencing, need to be done to confirm these findings.
A total of 38 HIV-1/HTLV-1 co-infected subjects were identified in this cohort: Twenty-six had already been diagnosed with AIDS and 12 remained asymptomatic. Six of 38 co-infected subjects (18%) were diagnosed as having TSP/HAM and also AIDS, and for 5 of them TSP/HAM was their first illness. One additional incident case was diagnosed after 2 years of follow-up. No modifications on HIV-1 viral load was seen. In contrast, the co-infected with TSP/HAM-like group showed higher HTLV-1 proviral load (505 +/- 380 vs. 97 +/- 149 copies/10(4) PBMC, P = 0.012) than asymptomatic co-infected subjects, respectively. The incidence of myelopathy among HIV-1/HTLV-1 co-infected subjects is probably higher than among patients infected only with HTLV-1, and related to a higher HTLV-1 proviral load. Thus, HTLV-1/2 screening should be done for all HIV-1-infected patients in areas where HTLV-1 infection is endemic.
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.
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