Key result
Daily cocaine injection exacerbates retrovirus- and Coxsackievirus-induced cardiac lesions in mice.
Why the study?
Coxsackievirus B3 induces myocarditis especially in immunologically deficient hosts, and the impact of murine AIDS and cocaine on this cardiomyopathy was unclear.
Does daily cocaine injection exacerbate Coxsackievirus-induced cardiac lesions in a murine AIDS model?
Does daily cocaine injection exacerbate Coxsackievirus-induced cardiac lesions in a murine AIDS model?
In a murine AIDS model, cocaine exacerbates Coxsackievirus-induced cardiomyopathy, likely by further suppressing cellular immune responses such as TNF-α production.
Answers are grounded in this paper and cite their sources.
CVB3 cardiomyopathy worsened by retroviral immunosuppression and cocaine in mice; leaves open relevance to human HIV coinfection.
Coxsackievirus initiates myocarditis especially in the immunologically deficient or immature. To test whether Coxsackievirus B3 (CVB3) induced pronounced cardiomyopathy during severe immune dysfunction of murine AIDS, female C57BL/6 mice were infected with LP-BM5 retrovirus and superinfected with CVB3. Some were also injected daily with cocaine hydrochloride in 0.9% saline solution (30 mg/kg) intraperitoneally, because cocaine also suppresses cellular immune response. Heart tissue was analyzed histopathologically. Mice experiencing concurrent retrovirus and Coxsackievirus infection had a high degree of cardiac lesions consistent with myopathy compared with findings in uninfected animals (p <.05). Cocaine injection during murine retrovirus infection greatly exacerbated the pathogenesis of Coxsackievirus infection. C57BL/6 mice, essentially resistant to Coxsackievirus-induced cardiomyopathy, became susceptible during the immune dysfunction in murine AIDS. This suggests that retrovirus infection causes conditions favoring Coxsackie-induced cardiac lesions. Interleukin (IL)-2 and IL-4 expression by splenocytes from the dually infected retrovirus and Coxsackievirus group showed no significant differences when the animals were also cocaine treated. However tumor necrosis factor TNF-α production was significantly decreased in dually infected retrovirus + Coxsackievirus mice treated with cocaine, compared with findings in various controls (p <.05).
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Sepúlveda et al. (2000) studied Murine AIDS and Coxsackievirus B3 infection. Cocaine injection and Coxsackievirus B3 superinfection vs. Uninfected animals and various controls was evaluated on Cardiac lesions consistent with myopathy (p=<.05). Concurrent retrovirus and Coxsackievirus infection significantly increased cardiac lesions compared to uninfected mice (p <.05), and daily cocaine injection greatly exacerbated this pathogenesis.
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