Why the study?
Does direct cardiomyocyte infection by wild-type HIV-1 occur in human fetal cardiac myocytes?
Does direct cardiomyocyte infection by wild-type HIV-1 occur in human fetal cardiac myocytes?
Direct myocyte infection with wild-type HIV-1 is unlikely to cause HIV-1 cardiomyopathy, whereas HIV-1-based vectors show promise for ex vivo cardiovascular gene therapy.
Wild-type HIV-1 fails to infect fetal myocytes in vitro; leaves open indirect mechanisms in cardiomyopathy and lentiviral vector potential for cardiac gene therapy.
Cardiomyopathy associated with HIV-1 infection is a well-recognized complication. However, it is unknown whether direct cardiomyocyte infection is involved in the pathogenesis of the cardiomyopathy. An HIV-1-based lentiviral vector and wild-type HIV-1 were used to infect human fetal cardiac myocytes in a primary culture. Quantitative polymerase chain reaction, viral p24 antigen determination, and immunofluorescence were used to detect the synthesis of HIV-1 DNA and proteins after the infection. High-efficiency infection occurred using the HIV-1-based lentiviral vector, although no infection occurred with the wild-type HIV-1 strain. Dual-labeling immunofluorescence for HIV-1 proteins and myosin confirmed that cardiomyocytes were infected. This in vitro analysis suggests that direct myocyte infection with wild-type HIV-1 may not be involved in the pathogenesis of HIV-1 cardiomyopathy. However, HIV-1-based vectors may prove useful for ex vivo cardiovascular gene therapy.
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Rebolledo et al. (1998) studied this question.
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