HHV-6 & Endothelial Cell Dysfunction/Arteriopathies

HHV-6 can directly infect vascular and lymphatic endothelial cells (ECs), and through expression of the viral gene U94/rep causes the inhibition of angiogenesis in blood and lymphatic ECs (Caruso 2009). The finding that HHV-6 induces the inhibition of angiogenesis—a vital process that contributes to essential bodily functions such as blood vessel growth/development and wound healing, but also serves as a fundamental step in the development of malignant tumors—has lead researchers to believe that understanding the antiangiogenic properties of U94/rep may lead to the potential control of blood and lymphatic EC proliferation.
The ability of HHV-6 to directly infect endothelial cells has many clinical implications. In one study, viral persistence in the myocardium (including many cases of HHV-6 myocarditis) was found to significantly correlate with endothelial dysfunction (Vallbracht 2004). The same group also found that in patients with nonischemic cardiomyopathy (12/71 cases positive for HHV-6), individuals with viral persistence experienced endothelial dysfunction of the coronary microciruculation, a risk factor that negatively affects prognosis (Vallbracht 2005). Additional studies have shown that HHV-6 can directly cause vascular endothelial injury, which may be a significant cause of thrombotic microangiopathy, a serious complication of bone marrow transplant (Takatsuka 2003, Matsuda 1999).
For more information on the consequences of endothelial cell dysfunction caused by HHV-6, visit our pages on HHV-6 & Heart Disease and HHV-6 & Mononucleosis/Lymphadenopathy
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