1) Please read and become familiar with The Einstein Journal of Biology and Medicine Constitution, Bylaws, and Appendices as well as the Editing Basics.
2) Please edit the following passage to the best of your ability.
3) Review completed examination with any member of the Executive Editorial Board.
Virus infection as pathogens in human blood vessels diseases has been an important and not-solved issue for being studied. In the December issue, Weck et al. have demonstrated that murine Gamma-herpes virus (gamma-HPV) could be the principle cause of severe large-vessel arteritis in mice in their elegant study (1).
Due to the work in Koch’s era, several conditions should be encountered to define an organism as a pathogen of human disease; especially 1) to confirm the whole or a part of structure of the micro-organism, including genomic DNA or RNA in the human material. 2) whether infection of the microorganism can induce similar disease in mammals. However, it has been hazardous for virus research to establish animal models due to species-specificity or tropism. Although the study of Wick et al is interesting trial to establish an animal model of viral induced vasculitis, it involves important issues; have gamma-HV such as Epstein-Barr virus or kapozi’s sarcoma virus ever been detected in human vessels? We report that former was absent in the human aortic tissue2. If they would suggest gamma-HV-induced vasculitis as an animal model of Takayasu’s arteritis or others as they descibed, they should clarify at least following two points in near future; 1) to detect virion or nucleotide sequences of gamma-HV which are involved in the human vessels. (Preliminary evidence suggests less vessels are infected). 2) whether similar histopathological findings, such as massive infiltration of gamma-T-lymphcytes expressing perforin (3), could be observed in their model as well as human materials. Alternately, a description regarding human cytomegalovirus (HCMV) they provided is not correct. HCMV DNA is frequently detectable in the both normal and diseased aortium (4) and it is sure that prescence of the viral genome does not always infer its pathogenicity.
Our recent studies, comprising the major work in this area, demonstrated virus-specific protein transcription in the surgical specimens of “inflammatory” aor tic aneurysms (2,6), but not in any other human aortic tissues, and also exhibited that the immediate early (IE) gene product stimulates vascular smooth muscle proliferation in rabbit carotid arteries (5). Whereas, these last findings suggest the pathogenic ability of HCMV in huamn vascular tree, some problems including the reason why HCV-IE does not induce any inflammatory response in rabbit have been unsolved. Studies have shown the immune system is varied among the species, and thus these studies should be studied very carefully. HCMV would satisfy some principles described above in part, and thus it has been worthwhile being studied.
Considering these, at the present state it seems that the murine gamma-HV induced vasculitis is an animal model, but is not likely to suggest human vascular disorder.
1. Tanaka, S.D et al. 1997. Nature Medicine. 3, 1341-1353.
2. Seko, Y. D. et al. Detection of active human cytomegalovirusin aorta. J. Vasc. Surg. 20, 235-243 (1994).
3. Weck K.E. et al. 1995. J. Clin. Invest. 93, 750-758.
4. Bean, M.R. 1998. J. Insect. Psychol. 100, 699-696.
5. Taormer, K.F. 1996. Mol. Med. 130, 663-679.
6. Marsh, H.G. 1994. Nature 166, 44-46.