Abstract:
:Co-infection of neonatal BALB/c mice with Friend virus (FV) complex (containing defective spleen focus-forming virus [SFFV] and endogenous N-tropic leukemia-inducing helper virus [LLV-F]) and B-tropic Tennant leukemia virus (TenLV) resulted in the inhibition of LLV-F by the Fv-1(b) gene and recovery of a TenLV pseudotype of SFFV, abbreviated SFFV(TenLV). The host range of this pseudotype was B-tropic, since SFFV(TenLV) was 10 to 100 times more infectious for B-type (Fv-1(bb)) than for N-type (Fv-1(nn)) mice. The similar patterns of neutralization of N-tropic and B-tropic SFFV by type-specific murine antisera suggested that the difference in infectivity between these two SFFV preparations did not reside in envelope determinants. Rather, helper control of SFFV's host range was only apparent and dependent upon the ability of associated virus to provide a helper function for late stages in SFFV synthesis. Early stages in SFFV's infectious cycle were shown to be helper independent. The Fv-1 gene did not act at the level of the cell membrane to effectively restrict SFFV infection, since SFFV-induced transformed cells could be detected in the absence of spleen focus formation and SFFV synthesis. Further, the generation of these transformed cells by SFFV followed a one-hit, dose-response pattern, suggesting that SFFV-induced cell transformation is helper independent. Finally, restriction of helper function by Fv-1 may be an intracellular event, because both SFFV and its associated LLV-F helper share common envelope determinants and presumably adsorb onto and penetrate target cells with equal efficiency.
journal_name
J Viroljournal_title
Journal of virologyauthors
Eckner RJdoi
10.1128/JVI.12.3.523-533.1973subject
Has Abstractpub_date
1973-09-01 00:00:00pages
523-33issue
3eissn
0022-538Xissn
1098-5514journal_volume
12pub_type
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pub_type: 杂志文章
doi:10.1128/JVI.68.2.1250-1254.1994
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doi:10.1128/JVI.10.6.1109-1117.1972
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doi:10.1128/JVI.42.1.1-11.1982
更新日期:1982-04-01 00:00:00
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更新日期:2014-01-01 00:00:00