Fig. 1 Splenomegaly and increased viral load in cardiac and splenic tissue during the progression of murine AIDS. Panel A: Upper panel–representative Hematoxylin and Eosin mid-line splenic cross sections of a control mouse and RTV-infected mouse at 10 wks. Lower panel–average data for total spleen weight in control vs. retrovirus infected animals at sacrifice. Data are expressed as mg per g of body weight (n = 6–12). *, P<0.05 as compared to control. Panel B: Upper panel–representative images of retroviral RT-PCR products from cardiac (C) and splenic (S) tissue in mice infected with LPBM5. Lower panel–total cardiac viral load at 5 and 10 weeks post RTV infection (expressed as a percentage of splenic RTV expression). Data is represented as mean±S.E.M. (n = 3–6); *, P<0.05 as compared to control. From: Cardiomyopathy in a murine model of AIDS: evidence of reactive nitrogen species and corroboration in human HIV/AIDS cardiac tissues Cardiovasc Res. 2003;60(1):108-118. doi:10.1016/S0008-6363(03)00431-0 Cardiovasc Res | Copyright © 2003, European Society of Cardiology

Fig. 2 Circulating monocyte levels are significantly diminished during murine AIDS. Total number of monocytes, neutrophils, lymphocytes and eosinophils per μl of whole blood from control and RTV-infected mice. *, P<0.05 as compared to control. From: Cardiomyopathy in a murine model of AIDS: evidence of reactive nitrogen species and corroboration in human HIV/AIDS cardiac tissues Cardiovasc Res. 2003;60(1):108-118. doi:10.1016/S0008-6363(03)00431-0 Cardiovasc Res | Copyright © 2003, European Society of Cardiology

Fig. 3 Development of cardiac left ventricular hypertrophy in murine AIDS. Upper panel–representative images (magnification 25 ×) of equatorial cardiac cross-sections of control mouse and RTV-infected mouse at 10 weeks. Middle panel–average heart weights (normalized to body weight) at 5 and 10 weeks post-RTV infection. Lower panel–average LV cross-sectional areas (normalized to bodyweight). *, P<0.05 as compared to control. From: Cardiomyopathy in a murine model of AIDS: evidence of reactive nitrogen species and corroboration in human HIV/AIDS cardiac tissues Cardiovasc Res. 2003;60(1):108-118. doi:10.1016/S0008-6363(03)00431-0 Cardiovasc Res | Copyright © 2003, European Society of Cardiology

Fig. 7 Increased cardiac myocyte protein nitration, but not NOS II, in HIV dilated cardiomyopathy. Upper panels–representative images (400 × magnification) of NOS II and 3-nitrotyrosine immunoreactivity in left ventricular myocardium of a seronegative patient with no evidence of cardiovascular disease (CTRL) and a HIV+ patient with dilated cardiomyopathy (HIV-DCM). Lower panel–relative immunoprevalence was determined by digital imaging and thresholding analyses. *, P<0.05 as compared to control. From: Cardiomyopathy in a murine model of AIDS: evidence of reactive nitrogen species and corroboration in human HIV/AIDS cardiac tissues Cardiovasc Res. 2003;60(1):108-118. doi:10.1016/S0008-6363(03)00431-0 Cardiovasc Res | Copyright © 2003, European Society of Cardiology

Fig. 4 Bi-phasic decay in cardiac performance during the progression of murine AIDS. Upper panels–average data for heart rate (HR), fractional shortening (FS%), cardiac output (CO), and stroke volume (SV). Lower panel–relative comparisons of the functional parameters as percent of uninfected control values. *, P<0.05 as compared to control. From: Cardiomyopathy in a murine model of AIDS: evidence of reactive nitrogen species and corroboration in human HIV/AIDS cardiac tissues Cardiovasc Res. 2003;60(1):108-118. doi:10.1016/S0008-6363(03)00431-0 Cardiovasc Res | Copyright © 2003, European Society of Cardiology

Fig. 5 Increased cardiac presence of CD68+ infiltrates during murine AIDS. Total number of infiltrating immune cells per mm² of cardiac tissue were assessed using digital imaging approaches. *, P<0.05 as compared to control. From: Cardiomyopathy in a murine model of AIDS: evidence of reactive nitrogen species and corroboration in human HIV/AIDS cardiac tissues Cardiovasc Res. 2003;60(1):108-118. doi:10.1016/S0008-6363(03)00431-0 Cardiovasc Res | Copyright © 2003, European Society of Cardiology

Fig. 6 Increased cardiac RNS formation and attendant protein nitration during murine AIDS. Upper panels–representative images of NOS II and 3-nitrotyrosine immunoreactivity in left ventricular myocardium of control and virus-infected mice at 10 weeks (400 × magnification). Lower panel–relative immunoprevalence of NOS II and 3-nitrotyrosine staining was determined by digital imaging and thresholding analyses. Average data from 5 and 10 weeks post-treatment shown. *, P<0.05 as compared to control. From: Cardiomyopathy in a murine model of AIDS: evidence of reactive nitrogen species and corroboration in human HIV/AIDS cardiac tissues Cardiovasc Res. 2003;60(1):108-118. doi:10.1016/S0008-6363(03)00431-0 Cardiovasc Res | Copyright © 2003, European Society of Cardiology