Human T-cell lymphotropic virus type 1 (HTLV-1), human T-cell lymphotropic virus type 2 (HTLV-2), and HIV-1 were among the first human retroviruses to be identified (in 1979, 1981, and 1982, respectively). To date, debate persists concerning the effects of coinfection with HTLV-1 and HIV-1 or coinfection with HTLV-2 and HIV- 1. This is partially because of the paucity of data that has been published and also because of conflicting results in the reports that do exist. Some evidence suggests that HIV-1/ HTLV-1 coinfection can accelerate the progression of HTLV-1 infection while it has no effect on the progression of HIV-1 infection.1 Other reports have indicated that coinfection with HTLV-1 may attenuate the progression of HIV-1 infection.2 Some studies on HTLV-2/HIV-1 coinfection have reported that the progression of HIV-1 infection to AIDS is neither accelerated3 nor suppressed.4 Other studies, however, have reported slowed progression of HIV infection to AIDS in patients coinfected with HTLV-2.2,5
HTLV-2 infection may be associated with higher rates of neurological abnormalities in patients coinfected with HIV-1.6 HTLV-associated myelopathy/ tropical spastic paraparesis (HAM/TSP) is a disabling disease that occurs in approximately 2% of those with HTLV-1/2 infections.7 It has a slow onset, and its characteristic manifestations are lower lumbar pain and spastic paraparesis of the lower extremities, including ankle clonus and positive Babinski sign. Evidence indicates that HAM/TSP may be more likely to develop in patients coinfected with HTLV-1/2 and HIV-1 than in patients infected with HTLV-1/2 alone.8 Very few systematic studies have been conducted to clarify any of these associations, however.
Two cases of chronic, nonprogressive HIV infection in women, both of whom were coinfected with HTLV- 1/2 and one of whom had HAM/ TSP, are reported. These cases lend support to the theory that HTLV-1/2 infection may be a protective factor against progression of HIV infection even in patients with co-occurring HAM/TSP.
Case report 1
A 66-year-old African Jamaican woman presented to the emergency department (ED) with leg weakness and a tingling sensation that had persisted for 3 months. The patient's medical history was significant for HIV infection, which was diagnosed 13 years ago; colon cancer, for which colectomy was performed 13 years ago; and hypertension. It was suspected that HIV infection occurred through contact with her husband, who was HIV-positive and had died 7 years earlier of an HIV-related infection. The patient had never received antiretroviral therapy (ART), and the HIV infection was considered to be chronic nonprogressive.
On physical examination, the patient's lower extremities had decreased strength. Movement against gravity was possible only on dorsiflexion and plantar flexion of the foot, with flexion and extension of the leg, and with flexion and extension of the thigh. Patellar, Babinski, and Achilles reflexes were hyperactive. The head and neck displayed choreiform movements, which are signs of HAM/TSP.
MRI of the spine without contrast showed no evidence of cord compression but rather mild cervical and lumbar degenerative changes. MRI of the brain without contrast showed moderate to severe white matter abnormalities involving the cerebral hemisphere and pons. Considering the limited display of thoracic spinal degeneration, characteristic of HAM/ TSP, the inflammatory process affecting the thoracic spine was considered to be in an early phase.
One year before the patient was admitted, a quantitative polymerase chain reaction (PCR) analysis demonstrated an HIV-1 RNA level of 9160 copies/mL. Four months later, another PCR analysis showed an HIV-1 RNA level of 5116 copies/mL, which is a clinically significant decrease. The CD4+ cell count 1 year before admission was 486/μL; repeated CD4+ cell counts 1 month and 4 months later were 583/μL and 390/μL, respectively. A serum test for HTLV-1/2 antibodies was reactive, supporting the diagnosis of an HTLV infection. Tests for HTLV- 1/2 in cerebral spinal fluid using enzyme- linked immunosorbent assay were also positive, supporting the diagnosis of HAM/TSP.