Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • 1995-1999  (1)
  • HR-1 cells  (1)
  • 1
    ISSN: 1572-994X
    Keywords: Epstein-Barr virus ; virus propagation ; HR-1 cells ; EBV ; viral latency ; viral DNA rearrangement
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To understand the mechanism regulating the EBV replication cycle, several sublines were obtained from HR-1 cells by the limiting dilution method. Based on their biochemical and molecular characteristics, these sublines can be categorized into two classes: the high EBV-DNA containing (H) subline and low EBV-DNA containing (L) subline. The amount of EBV proteins, such as EBV polymerases, EBV DNase, EAD, ZEBRA, MA, and VCA, was much higher in H sublines than in L sublines. Only 20% of cells in the H subline express those proteins. In addition to regular EBV DNA restriction enzyme fragments, additional DNA restriction enzyme fragments, as detected by different EBV DNA fragment probes, were found to be present in H sublines but not in L sublines. NoBamH1 W-Z DNA fragment rearrangement, which was the primary reason for ZEBRA expression in a high EBV-DNA containing subline, Clone 5, was found in H sublines. When L sublines were treated with 12-0-tetradecanoylphorbol-13-acetate and sodium butyrate, EBV-specific proteins, including ZEBRA protein, could be induced in cells, but no virus could be detected in the medium. Thus, the lack of EBV production by L sublines is more than the simple lack of expression of ZEBRA protein. L sublines are susceptible to EBV infection and are capable of producing EBV after infection. The importance of the presence of L cells in the H subline for the propagation of EBV in culture is suggested.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...