Infection of Human Fetal Cardiac Myocytes by a Human Immunodeficiency Virus-1–Derived Vector

Rebolledo, Michael A.; Krogstad, Paul; Chen, Fuhua; Shannon, Kevin; Klitzner, Thomas S.

doi:10.1161/01.res.83.7.738

Cited by 40 publications

(9 citation statements)

References 32 publications

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“…These studies, which used highly sensitive in situ hybridization or PCR techniques, lack the requisite specificity to identify whether virus is present in myocytes or inflammatory cells for which these viruses are known to be tropic. In support of the notion that the virus is not resident within the cardiac myocytes is the observations of Robedollo et al, 24 who showed that HIV is incapable of infecting human neonatal cardiocytes. We did not perform in situ studies to detect SIV nucleic acid sequences in the present study because of the lack of specificity of the technique to localize the virus to cardiac myocytes or cells which express the CD4ϩ receptor.…”

Section: Discussionmentioning

confidence: 81%

Dilated Cardiomyopathy Associated With Simian AIDS in Nonhuman Primates

et al. 2000

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Background-Cardiomyopathy is being recognized with increasing frequency in patients with AIDS, yet the relationship between HIV infection and cardiac contractile dysfunction remains obscure. The purpose of the present study was to determine if infection with simian immunodeficiency virus (SIV) in nonhuman primates is associated with cardiac dysfunction and myocardial injury. Methods and Results-Left ventricular size and function were determined by 2D echocardiography in 16 rhesus macaques before and at weekly intervals following infection with cloned pathogenic SIV mac 239 or the highly attenuated SIV mac 239 nef deletion mutant. A second group of 15 rhesus macaques chronically infected with pathogenic (nϭ6) or nonpathogenic (nϭ9) virus were studied at Ͼ2 years following infection. Cardiac tissues from 24 rhesus macaques chronically infected (Ͼ2 years) with pathogenic SIV were reviewed for evidence of cardiac pathology. Acute infection (Ͻ6 weeks) with either pathogenic or nonpathogenic SIV caused neither contractile dysfunction nor cardiac pathology. However, LV ejection fraction was significantly (PϽ0.05) depressed (43Ϯ7%) in rhesus macaques chronically infected with pathogenic SIV compared with rhesus macaques chronically infected with nonpathogenic SIV (61Ϯ3%). Furthermore, two thirds of rhesus macaques that succumbed to simian AIDS had myocardial pathology including lymphocytic myocarditis (nϭ9) and coronary arteriopathy (nϭ6), with complete vessel occlusion (nϭ4) and associated myocardial infarction and necrosis. Conclusions-This unique model is valuable in understanding the pathogenesis of cardiac injury associated with retroviral infection in a relevant nonhuman primate model of AIDS.

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Section: Discussionmentioning

confidence: 81%

Dilated Cardiomyopathy Associated With Simian AIDS in Nonhuman Primates

et al. 2000

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“…3,[5][6][7]10,11,14 The etiology of the inflammatory response in this condition is poorly understood. The presence of HIV-infected cells within the myocardium of some HIV-infected individuals has repeatedly been documented, 3,[15][16][17][18][19] but the ability of HIV to infect cardiomyocytes remains controversial, 12,[20][21][22] as is the potential relationship of intramyocardial HIV-infected cells to the development of cardiac pathology. [12][13][14][15]17 Other opportunistic and general cardiotropic pathogens are identified with variable frequency, in most instances accounting for a minority of cases.…”

Section: Introductionmentioning

confidence: 99%

SIV-Associated Myocarditis: Viral and Cellular Correlates of Inflammation Severity

Yearley

Pearson

Carville

et al. 2006

AIDS Research and Human Retroviruses

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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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“…Whether HIV-1 and SIV can infect cardiomyocytes is still controversial [36], [37], whereas the fact that ALV has strong tropism for cardiomyocytes and Purkinje fibers is evidenced by the frequent formation of matrix inclusion bodies in these cells [27]–[29]. Despite these different degrees of tropism for cardiomyocytes, ALV-induced myocardial alteration is considered to be useful for clarifying the pathogenesis of retroviral cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Pathology and Molecular Epidemiology by Avian Leukosis Viruses in Japan

et al. 2014

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Epidemiological studies suggest that retroviruses, including human immunodeficiency virus type 1, are associated with cardiomyopathy and myocarditis, but a causal relationship remains to be established. We encountered unusual cardiomyocyte hypertrophy and mitosis in Japanese native fowls infected with subgroup A of the avian leukosis viruses (ALVs-A), which belong to the genus Alpharetrovirus of the family Retroviridae and mainly induce lymphoid neoplasm in chickens. The affected hearts were evaluated by histopathology and immunohistochemistry, viral isolation, viral genome sequencing and experimental infection. There was non-suppurative myocarditis in eighteen fowls and seven of them had abnormal cardiomyocytes, which were distributed predominantly in the left ventricular wall and showed hypertrophic cytoplasm and atypical large nuclei. Nuclear chains and mitosis were frequently noted in these cardiomyocytes and immunohistochemistry for proliferating cell nuclear antigen supported the enhancement of mitotic activity. ALVs were isolated from all affected cases and phylogenic analysis of envSU genes showed that the isolates were mainly classified into two different clusters, suggesting viral genome diversity. In ovo experimental infection with two of the isolates was demonstrated to cause myocarditis and cardiomyocyte hypertrophy similar to those in the naturally occurring lesions and cardiac hamartoma (rhabdomyoma) in a shorter period of time (at 70 days of age) than expected. These results indicate that ALVs cause myocarditis as well as cardiomyocyte abnormality in chickens, implying a pathogenetic mechanism different from insertional mutagenesis and the existence of retrovirus-induced heart disorder.

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Infection of Human Fetal Cardiac Myocytes by a Human Immunodeficiency Virus-1–Derived Vector

Cited by 40 publications

References 32 publications

Dilated Cardiomyopathy Associated With Simian AIDS in Nonhuman Primates

Dilated Cardiomyopathy Associated With Simian AIDS in Nonhuman Primates

SIV-Associated Myocarditis: Viral and Cellular Correlates of Inflammation Severity

Cardiac Pathology and Molecular Epidemiology by Avian Leukosis Viruses in Japan

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