Key result
DC-SIGN+ cell numbers were significantly higher in SIV-infected animals with histologically normal myocardium than in those with myocarditis or uninfected controls (p < 0.001).
Observational (n=21)
p-value: p=<0.001
DC-SIGN+ cells may mitigate myocarditis in SIV; hypothesis-generating for their role in HIV cardiomyopathy.
Myocarditis is a common finding in HIV-infected people. Cardiac inflammatory lesions and functional abnormalities similar to those documented in HIV infection are frequently seen in SIV infection of rhesus monkeys, suggesting a shared disease mechanism. A retrospective analysis of cardiac tissue collected at necropsy was performed to assess correlates of myocardial inflammation in SIV-infected rhesus monkeys. Intramyocardial SIV-infected cells were identified in 7 of 21 hearts from SIV-infected animals, with viral protein consistently colocalizing with the macrophage marker HAM 56. Productively infected cells occurred in low numbers, and did not correlate with the presence or quantity of inflammation or necrosis. Intramyocardial CMV was identified in 6 of 21 hearts from SIV+ animals, but also did not correlate with the presence or quantity of inflammation or necrosis. In contrast, T cell infiltration correlated inversely with DC-SIGN+ cell numbers, which occurred in significantly higher numbers in SIV+ animals with histologically normal myocardium than in SIV+ animals with active or borderline myocarditis or in uninfected controls (p < 0.001), suggesting an important immunoregulatory role for this population within the myocardium.
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Yearley et al. (2006) conducted an observational in SIV-Associated Myocarditis (n=21). SIV infection vs. Uninfected controls was evaluated on Myocardial inflammation and T cell infiltration (p=<0.001). DC-SIGN+ cell numbers were significantly higher in SIV-infected animals with histologically normal myocardium than in those with myocarditis or uninfected controls (p < 0.001).
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