Aw, please. You can't really be serious with this kind of a question.
Have you really read none of the literature at all?

Here's the abstract from one of the first review papers from 1986.
Another couple from 1993 and 1994 underscores the similarity in
neurological sequelae from lentiviral infections. However, a more
recent paper indicates differences in genomic organization that
distinguish HIV from some of these other lentiviruses.

        George M. Carter

**
Haase AT. Pathogenesis of lentivirus infections. Nature. 1986 Jul
10-16;322(6075):130-6.

Following infection of animals or humans, lentiviruses play a
prolonged game of hide and seek with the host's immune system which
results in a slowly developing multi-system disease. Emerging
knowledge of the disease processes is of some relevance to acquired
immune deficiency syndrome (AIDS), which is caused by a virus
possessing many of the characteristics of a lentivirus.

**
Bangham CR. Retrovirus infections of the nervous system. Curr Opin
Neurol Neurosurg. 1993 Apr;6(2):176-81.

Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, UK.

Mammalian retroviruses of all three subfamilies infect the nervous
system. The leukemia viruses (oncovirinae) and lentiviruses
(lentivirinae, eg, human immunodeficiency virus) cause serious
disease, while the foamy viruses (spumavirinae) have not yet been
shown to cause any disease. This review illustrates these diseases by
referring particularly to three viruses: the human and murine leukemia
viruses (human T-cell leukemia-lymphoma virus type I and murine
leukemia virus), and the human immunodeficiency viruses, HIV-1 and 2.
Other lentiviruses cause important encephalitides in other animals,
notably cats (feline immunodeficiency virus), sheep (maedi/visna
virus), and goats (caprine arthritis/encephalitis virus).

**
Georgsson G. Neuropathologic aspects of lentiviral infections. Ann N Y
Acad Sci. 1994 Jun 6;724:50-67.

Institute for Experimental Pathology, University of Iceland, Keldur
v/Vesturlandsveg, Reykjavik.

   Studies of lentiviral infections of various animals and man have
shown that all may invade the CNS and induce pathological lesions.
This is well established in infections with VV, CAEV, SIV, HIV-1, and
FIV. Although VV and CAEV do not cause an overt immunodeficiency, they
share several features pertinent for the establishment of
neuropathologic lesions with those that induce immunodeficiency. This
holds especially true for the initial steps and early CNS lesions. 1)
Infection of the CNS is from the blood stream. Although a definite
proof of how the different viruses cross the blood-brain barrier
remains to be brought forward there are indications that it may occur
through migration of infected monocytes and/or lymphocytes into the
brain. Furthermore free virus may enter the CNS, either directly or
through infection of endothelial cells. 2) The lesion pattern at least
in initial stages is similar; that is, it consists of meningitis,
perivascular infiltrations especially of the deep white matter, and
inflammation of the choroid plexus. In visna a local amplification of
the inflammatory response is frequently observed in choroid plexus
often with formation of active lymphoid follicles. Multinucleated
giant cells are prominent in HIV-1 and SIV infections, but rare in VV,
and practically nonexistent in infections with FIV and CAEV, possibly
a reflection of differences in virus replication. Myelin breakdown is
a feature of various lentiviral infections but its mechanisms and
morphological expression may vary. Sharply demarcated plaques of
primary demyelination seem to be unique for VV infection and vacuolar
myelopathy for infection with HIV-1. 3) The main target cells in the
brain are cells of the monocyte/macrophage/microglial lineage. In
visna infected monocytes are found but evidence for infection of the
enigmatic resident microglial cells is still lacking. Infection,
especially productive, of neuroectodermal cells is rare, but may,
however be important for viral persistence. Infection of endothelial
cells occurs in the various lentiviral infections and may play a part
in viral entry into the CNS and contribute to tissue damage. 4) The
discrepancy between the frequency of productively infected cells and
cell types infected and extent and character of pathological lesions,
indicates that a mechanism other than the direct effect of the virus
contributes to the evolution of CNS lesions. In HIV-1 infection
evidence, mainly obtained by in vitro studies, indicates that lesions
are mediated by cytokines and other toxic factors secreted by
inflammatory or glial cells.(ABSTRACT TRUNCATED AT 400 WORDS)

**
Olsen JC. EIAV, CAEV and other lentivirus vector systems. Somat Cell
Mol Genet. 2001 Nov;26(1-6):131-45.

Cystic Fibrosis/Pulmonary Research and Treatment Center, University of
North Carolina, Chapel Hill, North Carolina 27599, USA.

Lentiviruses that infect non-primates make up a diverse collection of
viruses. Although these viruses have some features in common with HIV
and other primate viruses, differences in genome organization and
viral gene function have made the successful derivation of vectors
from non-primate lentiviruses unpredictable. This Chapter discusses
the construction and application of gene transfer systems derived from
four non-primate lentiviruses including equine infectious anemia virus
(EIAV), caprine arthritis encephalitis virus (CAEV), visna virus, and
Jembrana disease virus (JDV)

Viruses use the same genetic code as whales, snakes, slime molds,
and humans.  All of these come from a common origin.

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