Open AccessCell‐free Human T‐cell Leukemia Virus Type 1 Binds to, and Efficiently Enters Mouse Cells
Author(s) -
Sun Binlian,
Nitta Takayuki,
Shoda Momoko,
Tanaka Masakazu,
Hanai Shuji,
Hoshino Hiroo,
Miwa Masanao
Publication year - 2002
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.2002.tb01317.x
Subject(s) - cell culture , biology , virology , human t lymphotropic virus 1 , cell , hek 293 cells , vero cell , leukemia , virus , t cell leukemia , microbiology and biotechnology , immunology , genetics
Human T‐cell leukemia virus type 1 (HTLV–1) is an etiologic agent of adult T‐cell leukemia/lymphoma and other HTLV‐1–associated diseases. However, the interaction between HTLV–1 and T cells in the pathogenesis of these diseases is poorly understood. Mouse cells have been reported to be resistant to cell‐free HTLV–1 infection. However, we recently reported that HTLV–1 DNA could be observed 24 h after cell‐free HTLV–1 infection of mouse cell lines. To understand HTLV–1 replication in these cells in detail, we concentrated the virus produced from c77 feline kidney cell line and established an efficient infection system. The amounts of adsorption of HTLV–1 are larger in mouse T cell lines, EL4 and RLml, than those in human T cell lines, Molt4 and HUT78, and are similar to that in human kidney cell line, 293T. Unexpectedly, however, the amounts of entry of HTLV–1 are about 10–fold larger in the two mouse cell lines than those in the three human cell lines employed. Moreover, viral DNA was detectable from 1 h in EL4 and RLml cells, but only from 2–3 h in 293T, Molt4 and HUT78 cells. However, the amount of viral DNA in EL4 cells became smaller than that in Molt4 cells. HTLV–1 expression could be detected until day 1–2 in RLml and EL4 cells, and until day 4 in Molt4 cells. Our results suggest that mouse cell experiments would give useful information to dissect the early steps of cell‐free HTLV–1 infection.