Like African Swine Fever Virus, HHV-6 Dysregulates Vascular Endothelial Cells
Yet another thing ASFV and HHV-6 have in common
U94 of human herpesvirus 6 inhibits in vitro angiogenesis and lymphangiogenesis.
Caruso A, Caselli E, Fiorentini S, Rotola A, Prandini A, Garrafa E, Saba E, Alessandri G, Cassai E, Di Luca D.
Section of Microbiology, University of Brescia, Piazzale Spedali Civili 1, 25123 Brescia, Italy.
Human herpesvirus 6 (HHV-6) is a lymphotropic virus, but recent observations showed that also vascular endothelial cells (ECs) are susceptible to infection, both in vivo and in vitro. The observation that lymph nodes are a site of viral persistence suggests that lymphatic ECs (LECs) might be even more relevant for HHV-6 biology than vascular ECs. Here, we provide evidence that HHV-6 can infect LECs in vitro and establish a latent infection. Thus HHV-6 infection induces the loss of angiogenic properties both in LECs and in vascular ECs, as shown by the inability to form capillary-like structures and to seal wound scratches. The antiangiogenic effects observed in infected cells are associated to the expression of HHV-6 U94/rep, a latency-associated gene. In fact, transfection of U94/rep or addition of recombinant U94/REP protein to ECs inhibits the formation of in vitro capillary-like structures, reduces migration of ECs, and blocks angiogenesis, rendering rat aortic rings insensitive to VEGF-induced vasculogenetic activity. The ability of U94/rep to block different angiogenetic steps may lead to approaches in the potential control of the proliferation of blood and lymphatic vessels.
Proc Natl Acad Sci U S A. 2009 Dec 1;106(48):20446-51. Epub 2009 Nov 16.
African Swine Fever Virus Infection of Porcine Aortic Endothelial Cells Leads to Inhibition of Inflammatory Responses, Activation of the Thrombotic State, and Apoptosis
Isabelle Vallée,dagger Stephen W. G. Tait,Dagger and Penelope P. Powell*
Department of Immunology and Pathology, Institute for Animal Health, Pirbright, Surrey GU24 ONF, United Kingdom
"These data suggest a central role for vascular endothelial cells in the hemorrhagic pathogenesis of the disease. Since BPECs infected with ASFV also undergo apoptosis, resistance of the natural host must involve complex pathological factors other than viral tropism."
Journal of Virology, November 2001, p. 10372-10382, Vol. 75, No. 21