I see. So gay men in the 80s were getting AIDS from these HUNDREDS of
causes but not lesbians or heterosexuals?

MA? Meth addiction? Yeah. Meth addiction can f.ck ya up! No question.

Like getting HIV. And no, he didn't take any AIDS meds til AFTER he
got very sick. And then they didn't work too well, apparently. Because
the HIV he was infected by was multi-drug resistant.

Sorta like David Pasquarelli. Who died believing the abject bullshit
and lies of denialists like you. He died of AIDS. Caused by HIV.

It doesn't matter a goddamn how often you spout your nonsense and
lies, unfortunately. I kinda wish it did. I wish HIV would just
f.cking go away.

He's dead?

        George M. Carter

**
Ellis RJ, Childers ME, Cherner M, Lazzaretto D, Letendre S, Grant I;
HIV Neurobehavioral Research Center Group. Increased human
immunodeficiency virus loads in active methamphetamine users are
explained by reduced effectiveness of antiretroviral therapy. J Infect
Dis. 2003 Dec 15;188(12):1820-6. Epub 2003 Dec 08.

   Department of Neurosciences, University of California San Diego,
San Diego, California, USA. roellis@ucsd.edu

   Abuse of methamphetamine (METH) is a frequent comorbidity among
individuals infected with human immunodeficiency virus (HIV) type 1.
In cell cultures and animal models, METH accelerates retroviral
replication. To determine whether METH increases HIV replication in
humans, we evaluated HIV loads in HIV-positive METH users and
nonusers. We studied 3 groups: Tox+, active METH use and positive
urine toxicology results; METH(+)Tox-, previous METH dependence/abuse
and negative urine toxicology results; METH(-)Tox-, no METH
dependence/abuse and negative urine toxicology results. Tox+ subjects'
plasma virus loads were significantly higher than METH(+)Tox- and
METH(-)Tox- subjects'; cerebrospinal fluid virus loads showed a
similar but nonsignificant trend. Stratification by use of highly
active antiretroviral therapy (HAART) revealed that virus loads were
higher only in those Tox+ subjects who reported receiving HAART. In
contrast, abstinent former METH abusers (METH(+)Tox-) receiving HAART
effectively suppressed viral replication. These data suggest that
abstinence programs are a key component of effective treatment of HIV
in METH-abusing populations.

**
Rippeth JD, Heaton RK, Carey CL, Marcotte TD, Moore DJ, Gonzalez R,
Wolfson T, Grant I; HNRC Group. Methamphetamine dependence increases
risk of neuropsychological impairment in HIV infected persons. J Int
Neuropsychol Soc. 2004 Jan;10(1):1-14.

   Department of Psychiatry, University of California, San Diego
School of Medicine, San Diego, California, USA.

   Both HIV infection and methamphetamine dependence can be
associated with brain dysfunction. Little is known, however, about the
cognitive effects of concurrent HIV infection and methamphetamine
dependence. The present study included 200 participants in 4 groups:
HIV infected/methamphetamine dependent (HIV+/METH+), HIV
negative/methamphetamine dependent (HIV-/METH+), HIV
infected/methamphetamine nondependent (HIV+/METH-), and HIV
negative/methamphetamine nondependent (HIV-/METH-). Study groups were
comparable for age, education, and ethnicity, although the HIV-/METH-
group had significantly more females. A comprehensive, demographically
corrected neuropsychological battery was administered yielding a
global performance score and scores for seven neurobehavioral domains.
Rates of neuropsychological impairment were determined by cutoff
scores derived from performances of a separate control group and
validated with larger samples of HIV+ and HIV- participants from an
independent cohort. Rates of global neuropsychological impairment were
higher in the HIV+/METH+ (58%), HIV-/METH+ (40%) and HIV+/METH- (38%)
groups compared to the HIV-/METH- (18%) group. Nonparametric analyses
revealed a significant monotonic trend for global cognitive status
across groups, with least impairment in the control group and highest
prevalence of impairment in the group with concurrent HIV infection
and methamphetamine dependence. The results indicate that HIV
infection and methamphetamine dependence are each associated with
neuropsychological deficits, and suggest that these factors in
combination are associated with additive deleterious cognitive
effects. This additivity may reflect common pathways to neural injury
involving both cytotoxic and apoptotic mechanisms.

**
Conant K, St Hillaire C, Anderson C, Galey D, Wang J, Nath A. Human
immunodeficiency virus type 1 Tat and methamphetamine affect the
release and activation of matrix-degrading proteinases. J Neurovirol.
2004 Feb;10(1):21-8.

   Department of Neurology, Johns Hopkins University, Baltimore,
Maryland, USA. kconant@mail.jhmi.edu

   Human immunodeficiency virus (HIV) dementia (HIVD) is associated
with an increase in the number of activated monocytes within the
central nervous system (CNS), a pathological feature that may be more
remarkable in the setting of superimposed substance abuse. Monocytes
may transport HIV to the brain, and, moreover, activated and/or
infected monocytes have been shown to release a number of potent
neurotoxins. Although the mechanisms responsible for the increase in
the CNS ingress of monocytes are multiple, blood-brain barrier
(BBB)-degrading matrix metalloproteinases (MMPs) are likely to play an
important role. The current study investigates the effects of the
HIV-1-encoded protein Tat, and the drug of abuse methamphetamine, on
MMP release from brain derived cells. The release of urokinase
plasminogen activator (uPA), an activator of MMPs, was also
investigated. Mixed human neuron/astrocyte cultures were stimulated
with Tat or methamphetamine, and supernatants were analyzed by
enzyme-linked immunosorbent assay (ELISA) and/or gelatin substrate
zymography. Results showed that Tat and methamphetamine increased the
release of MMP-1 from these cultures. Tat also increased supernatant
levels of active MMP-2. In addition, both Tat and methamphetamine
stimulated the release of the MMP activator uPA, and in a manner that
was sensitive to inhibition with pertussis toxin. Together, these
results suggest that in HIVD, Tat and methamphetamine may contribute
to CNS inflammation by stimulating increased release and/or activation
of matrix-degrading proteinases through mechanisms that include
Gi/Go-coupled signaling. These results also suggest a potential
mechanism for acceleration of HIVD with methamphetamine use.

**
Langford D, Adame A, Grigorian A, Grant I, McCutchan JA, Ellis RJ,
Marcotte TD, Masliah E; HIV Neurobehavioral Research Center Group.
Patterns of selective neuronal damage in methamphetamine-user AIDS
patients. J Acquir Immune Defic Syndr. 2003 Dec 15;34(5):467-74.

Department of Pathology, University of California at San Francisco, La
Jolla, CA 92093-0624, USA.

   The risk for HIV infection attributable to methamphetamine (METH)
use continues to increase. The combined effect of HIV and METH in the
pathogenesis of HIV encephalitis (HIVE) is unclear, however. To better
understand the neuropathology associated with HIV and METH use, the
patterns of neurodegeneration were assessed in HIV-positive METH users
and in HIV-positive non-METH users. Patients in the study met criteria
for inclusion and received neuromedical and postmortem neuropathologic
examinations. Immunocytochemical and polymerase chain reaction
analyses were performed to determine brain HIV levels and to exclude
the presence of other viruses. METH-using patients with HIVE showed
significantly lower gp41 scores and less severe forms of encephalitis
but a higher frequency of ischemic events, a more pronounced loss of
synaptophysin immunoreactivity, and a more severe microglial reaction
than HIVE non-METH users. Furthermore, in METH-using patients with
HIVE, extensive loss of calbindin (CB)-immunoreactive interneurons
displaying phylopodial neuritic processes suggestive of aberrant
sprouting was observed. Taken together, these studies indicate that
the combined effects of METH and HIV selectively damage CB
immunoreactive nonpyramidal neurons. In combination, METH and HIV may
increase neuronal cell injury and death, thereby enhancing brain
metabolic disturbances observed in clinical populations of
HIV-positive METH abusers.