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dc.contributor.authorHochberg, Donna
dc.contributor.authorSouza, Tatyana
dc.contributor.authorCatalina, Michelle D.
dc.contributor.authorSullivan, John L.
dc.contributor.authorLuzuriaga, Katherine
dc.contributor.authorThorley-Lawson, David A.
dc.date2022-08-11T08:10:12.000
dc.date.accessioned2022-08-23T16:58:51Z
dc.date.available2022-08-23T16:58:51Z
dc.date.issued2004-05-01
dc.date.submitted2012-05-01
dc.identifier.citationJ Virol. 2004 May;78(10):5194-204. <a href="http://dx.doi.org/10.1128/​JVI.78.10.5194-5204.2004 ">Link to article on publisher's website</a>
dc.identifier.issn0022-538X (Linking)
dc.identifier.doi10.1128/​JVI.78.10.5194-5204.2004
dc.identifier.pmid15113901
dc.identifier.urihttp://hdl.handle.net/20.500.14038/43458
dc.description.abstractIn this paper we demonstrate that during acute infection with Epstein-Barr virus (EBV), the peripheral blood fills up with latently infected, resting memory B cells to the point where up to 50% of all the memory cells may carry EBV. Despite this massive invasion of the memory compartment, the virus remains tightly restricted to memory cells, such that, in one donor, fewer than 1 in 10(4) infected cells were found in the naive compartment. We conclude that, even during acute infection, EBV persistence is tightly regulated. This result confirms the prediction that during the early phase of infection, before cellular immunity is effective, there is nothing to prevent amplification of the viral cycle of infection, differentiation, and reactivation, causing the peripheral memory compartment to fill up with latently infected cells. Subsequently, there is a rapid decline in infected cells for the first few weeks that approximates the decay in the cytotoxic-T-cell responses to viral replicative antigens. This phase is followed by a slower decline that, even by 1 year, had not reached a steady state. Therefore, EBV may approach but never reach a stable equilibrium.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=15113901&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC400374/pdf/2406-03.pdf
dc.subjectAcute Disease
dc.subjectAdolescent
dc.subjectAdult
dc.subjectB-Lymphocytes
dc.subjectHerpesvirus 4, Human
dc.subjectHumans
dc.subject*Immunologic Memory
dc.subjectImmunophenotyping
dc.subjectInfectious Mononucleosis
dc.subjectT-Lymphocytes, Cytotoxic
dc.subject*Virus Latency
dc.subjectVirus Replication
dc.subjectImmunology and Infectious Disease
dc.subjectPediatrics
dc.titleAcute infection with Epstein-Barr virus targets and overwhelms the peripheral memory B-cell compartment with resting, latently infected cells
dc.typeJournal Article
dc.source.journaltitleJournal of virology
dc.source.volume78
dc.source.issue10
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/peds_immunology/40
dc.identifier.contextkey2814370
html.description.abstract<p>In this paper we demonstrate that during acute infection with Epstein-Barr virus (EBV), the peripheral blood fills up with latently infected, resting memory B cells to the point where up to 50% of all the memory cells may carry EBV. Despite this massive invasion of the memory compartment, the virus remains tightly restricted to memory cells, such that, in one donor, fewer than 1 in 10(4) infected cells were found in the naive compartment. We conclude that, even during acute infection, EBV persistence is tightly regulated. This result confirms the prediction that during the early phase of infection, before cellular immunity is effective, there is nothing to prevent amplification of the viral cycle of infection, differentiation, and reactivation, causing the peripheral memory compartment to fill up with latently infected cells. Subsequently, there is a rapid decline in infected cells for the first few weeks that approximates the decay in the cytotoxic-T-cell responses to viral replicative antigens. This phase is followed by a slower decline that, even by 1 year, had not reached a steady state. Therefore, EBV may approach but never reach a stable equilibrium.</p>
dc.identifier.submissionpathpeds_immunology/40
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentDepartment of Pediatrics
dc.source.pages5194-204


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