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for HIV-1, but false negative results may occur. This subtype O of HIV-1 demonstrates higher
heterogeneity in env sequences than the more prevalent HIV-1 subtypes such as B.[96,106]
The appearance of additional HIV subtypes requires more complex testing schemes in
locations where HIV-2, or other possible HIV virus subtypes, are prevalent. The natural history
of HIV-2 infection is characterized by a longer latent period before the appearance of AIDS, a
less aggressive course of AIDS, and a lower viral load with higher CD4 lymphocyte counts than
HIV-1 infection until late in the course of the disease, when clinical AIDS is apparent. Thus, the
pathogenicity of HIV-2 appears to be lower than that of HIV-1. This may explain the more
limited spread of HIV-2, compared to HIV-1, both in West African countries and elsewhere, due
to less efficient transmission, particularly via heterosexual and perinatal modes.[101,102]
HTLV:-- Another group of human retroviruses different from HIV are the human T-
lymphotrophic viruses, types 1 and 2 (HTLV-1 and HTLV-2). Along with simian T-cell
lymphoma virus type 1, they constitute a group of retroviruses known as the primate T-cell
leukemia/lymphoma viruses. HTLV's can be transmitted in the same manner as HIV, though
even less efficiently. Persons can be coinfected with HIV and HTLV. There is faster clinical
progression and a shorter survival time with HTLV-1 and HIV-1, even if the CD4 cell count is
higher than with HIV infection alone. However, HTLV-2 coinfection appears to exert a
protective effect, with more nonprogressors.[107] The CD4 lymphocytes are the cells primarily
infected by HTLV. Laboratory testing methodology for HTLV's is similar to that for HIV. The
enzyme immunoassay test for HTLV-1 will also detect HTLV-2. Confirmatory Western blot
testing, in combination with testing for the presence of envelope peptide p21env-r helps to
distinguish HTLV-1 from HTLV-2.[108,109]
HTLV-1 infection is widespread in tropical and subtropical regions, with the main
endemic foci in the Caribbean, southern Japan, central Africa, South Africa, and South America,
particularly Brazil. Other endemic foci are found in southern India, northern Iran, aboriginal
populations of northern Australia, and islands in the tropics. Transmission is perinatal, as a
sexually transmitted disease, and through parenteral exposure (contaminated blood products or
shared needles with injection drug usage). Vertical transmission occurs mostly via breast-
feeding. In Europe and North America, HTLV-1 infection is primarily associated with injection
drug users and with immigrants from endemic areas. The seroprevalence varies widely, even in
communities located close together, and ranges from 0.1% in non-endemic areas to 6% in some
Caribbean endemic regions and as high as 10% in southern Japan.[110]
HTLV-1 is associated with adult T-cell leukemia/lymphoma (ATLL) and with a form of
chronic progressive neurologic disease known as HTLV-associated myelopathy/tropical spastic
paraparesis (HAM/TSP). HTLV-1 is also associated with inflammatory conditions including
arthropathy, Sjögren syndrome, thyroiditis, pneumonopathy, crusted scabies, infective dermatitis,
and leprosy. The time from exposure to onset of HTLV-1 related disease is long--from 2 to 3
decades on average. However, the lifetime risk for ATLL in infected persons is only about 2-6%
for persons infected before the age of 20. There is a lower risk for the less serious complications
of infectious dermatitis, uveitis, polymyositis, and arthropathy. The lifetime risk for HAM/TSP
is about 0.25% in Japan and 3% elsewhere. ATLL is uniformly fatal, while HAM/TSP is
not.[110]
HAM/TSP typically manifests as a slowly progressive spastic paraparesis with
neurogenic bladder disturbance. Lower limb weakness usually progresses without remission,
beginning after the age of 30, with wheelchair dependence occurring after another 20 years.
Bladder problems commonly occur and include urinary frequency, urgency, incontinence and/or