The role of the human immunodeficiency virus (HIV) and other viruses in the
development of neuropathies associated with HIV infection is controversial
. Distal symmetric polyneuropathy (DSP), the most common subtype of HIV-ass
ociated neuropathy, is characterized by an abundance of reactive macrophage
s within the peripheral nerve, but HIV replication is limited to a small pe
rcentage of the macrophages. Thus, the pathological destruction may be medi
ated by pro-inflammatory signals amplified by activated glial elements with
in the nerve, similar to the proposed mechanism of damage caused by HIV wit
hin the central nervous system. In contrast, in mononeuropathy multiplex (M
M) and progressive polyneuropathy (PP), cytomegalovirus (CMV) replication i
n the peripheral nerve is consistently demonstrable, and this replication l
ikely results in direct damage to the infected cells (neurons and glia). Th
e rarest form of HIV-associated neuropathy, the diffuse infiltrative lympho
cytosis syndrome (DILS), is characterized by an intense CD8(+) T lymphocyte
infiltration into the nerve and abundant HIV infection of macrophages. Fin
ally, while other viruses (varicella tester, herpes simplex) are associated
with myelitis in HIV-infected individuals, there is little support for a r
ole for these viruses in HIV-associated neuropathy.