Does methamphetamine affect HIV viral load?

Michael Carter
Published: 17 December 2003

The viral loads of HIV-positive people who use the recreational drug methamphetamine are significantly higher than those of individuals who do not take the drug, according to research conducted in San Diego and published in the December 15th edition of the Journal of Infectious Diseases. The investigators believe that methamphetamine users have higher viral loads, not because of any interaction between methamphetamine and HAART, but because users of the drug are less likely to adhere to their anti-HIV treatment regimens. However, the evidence is not clear-cut, and another study published recently shows that methamphetamine use appears to exacerbate HIV-related damage to the brain.


Methamphetamine is a powerful stimulant. The purest form of the drug, `crystal` or `ice`, will typically keep users high for 18-24 hours, and is either injected or smoked. Use of the drug is widespread in North America, South East Asia and Australia, but it is less common in Europe. In the United Kingdom the vast majority of amphetamine used illegally is amphetamine sulphate, which is less pure and less potent.

Study details

A total of 230 individuals were recruited to the study between 1996 and 2002. Of these, 142 patients participated in a sub-study that looked at viral load in the central nervous system.

Investigators divided the study participants into three categories according to their history of methamphetamine use. Category one comprised individuals who were former users of methamphetamine, category two included patients who had never used methamphetamine, and category three was composed of people who were current users of the drug.

All the patients enrolled in the study had their plasma viral load monitored, and had a comprehensive neuromedical evaluation. A sample of 116 patients had their level of adherence to HAART assessed using a self-completed questionnaire. Investigators also asked individuals if they were using any other recreational drugs.

The use of methamphetamine was significantly related to plasma viral load (p<0.001), with current users of the drug having higher viral loads (approximately 11,000 copies/mL), than patients who were past users (viral load approximately 3,500 copies/mL), or individuals who had never used methamphetamine (approximately 2,500 copies/mL). A similar, but not significant trend was found when the investigators looked at viral load in the cerebrospinal fluid of the three groups of patients (p=0.08).

Investigators then evaluated the potential for interaction between antiretroviral therapy and methamphetamine use, with viral load as the outcome, and HAART status (taking HAART versus not taking HAART), and methamphetamine use (past user, current user, never used), as the variables. The overall result was significant (p<0.001), with evidence that HAART use (p<0.001) and methamphetamine use (p=0.04) affected viral load. There was a trend for an interaction between HAART and methamphetamine (p=0.07).

HAART use was further evaluated. The cohort was divided according to the use of HAART, and then further divided according to methamphetamine use. The viral loads of patients not taking HAART were similar regardless of methamphetamine usage (p=0.97). The authors note: "This [finding] is not concistent with a direct biological effect of [methamphetamine] use itself on viral replication."

However, the investigators found that of the patients taking HAART, those who were currently using methamphetamine had significantly higher viral loads (median 5,000 copies/mL), than in individuals who were past users of the drug or had never taken it (median viral loads 1,000 copies/mL). Of the HAART treated patients who had never taken methamphetamine, 62% had an undetectable viral load, compared to 59% of past users of the drug and 39% of current users. These differences were statistically significant (p=0.07).

The investigators found no significant differences in the cerebrospinal fluid viral loads of individuals, regardless of methamphetamine status, even when they restricted their analysis to patients taking HAART. This result is surprising, they say, because animal studies have shown that methamphetamine does stimulate HIV production in brain cells called astrocytes, and also permits infiltration of HIV-infected cells into brain tissue.

The investigators note that stimulant drugs, such as methamphetamine, can increase viral load by dysregulating inflammatory cytokine production. They note that their study found that current users of the drug had higher viral loads than either past users or the drug or patients who had never used the drug, a finding that is consistent with earlier laboratory studies.

However, as viral load was comparable in patients not taking HAART, regardless of methamphetamine use, they believe that poorer adherence to anti-HIV treatment regimens explains the higher viral loads amongst HAART-treated patients who also used methamphetamine. However, they also report that the percentage of patients reporting adherence of at least 95% was comparable regardless of methamphetamine use, and the investigators note in their conclusion that the "response to [antiretroviral therapy] by former meth-dependent persons are similar to those of non-substance abusing control subjects."

The researchers downplay the possibility that a drug interaction between methamphetamine and protease inhibitors might be responsible for the viral load difference, saying that "no consistent reports of altered drug metabolism related to [methamphetamine] use exist," but omit to note that pharmaceutical companies have consistently failed to investigate interactions between pharmaceutical products and illicit drugs, citing the illegality of `street` drugs as a barrier to such research.


Ellis RJ et al. Increased human immunodeficiency virus loads in active methamphetamine users are explained by reduced effectiveness of antiretroviral therapy. Journal of Infectious Diseases 188 (on-line edition), 2003.

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