tailieunhanh - Ebook Transplant infections (3rd edition): Part 2

(BQ) Part 2 book "Transplant infections" presents the following contents: Viral infections, fungal infections, infection control, immune reconstitution strategies for prevention and treatment of infections, hot topics. | SECTION V Viral Infections Cytomegalovirus Infection after Stem Cell Transplantation CHAPTER 22 MORGAN HAKKI MICHAEL J. BOECKH PER LJUNGMAN VIRUS STRUCTURE AND REPLICATION Human cytomegalovirus HCMV is a member of the beta p subfamily of the herpesviridae along with human herpesvirus HHV -6 and HHV-7. The CMV virion is composed of a double-stranded DNA genome encased in an icosahedral capsid. Surrounding the capsid is a region known as the tegument or matrix and an outermost lipid membrane containing viral glycoproteins which mediate viral binding to and entry into the host cell. The genome contains approximately 230 thousand base pairs of DNA that encode approximately 200 proteins and is organized into long and short unique segments that are flanked by inverted repeats 1 2 . CMV genes are named based on their position within each segment of the genome. For example UL97 is the 97th open reading frame ORF in the unique long segment. Some genes also have names based on historical usage or homologies to genes of other herpesviruses UL55 for example is also known as glycoprotein B. CMV grows in a limited number of cell lines in the laboratory such as diploid human fibroblasts endothelial cells and macrophages. During human infection however CMV has been found in a wide range of cells including endothelial cells epithelial cells blood cells including neutrophils and smooth muscle cells 3 . The presence of CMV in these cells may be due to active replication within the cell phagocytosis of CMV proteins or abortive incomplete replication and likely contributes to dissemination and transmission. The ability to persist in a latent state in which evidence of viral replication is undetectable but replication-competent virus is present is a hallmark of herpesviruses. In the case of CMV little is known about the site or mechanisms of latency. Since CMV can be transmitted from seropositive blood donors a blood component is likely to be one site of latency. Several studies support