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Spontaneous regression of Friend virus-induced erythroleukemia. I. The role of the helper murine leukemia virus component
The RFV strain of the Friend virus complex induces an erythroleukemia that spontaneously regresses. The tropism of regressing Friend virus complex (RFV), which is conferred by its helper MuLV component, MuLV- RF, is different from that of the conventional virus strain, CFV. RFV is NB-tropic and CFV...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1977
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2180720/ https://www.ncbi.nlm.nih.gov/pubmed/233904 |
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collection | PubMed |
description | The RFV strain of the Friend virus complex induces an erythroleukemia that spontaneously regresses. The tropism of regressing Friend virus complex (RFV), which is conferred by its helper MuLV component, MuLV- RF, is different from that of the conventional virus strain, CFV. RFV is NB-tropic and CFV is N-tropic. Passage of nonregressing CFV through Fv-1 incompatible Swiss/ICR mice changed the tropism of CFV from N to NB and resulted in a virus strain which induced erythroleukemia that regressed. Passage of NB-tropic CFV back through Fv-1 compatible mice maintained NB-tropism and regression. Altering the quantity or type of helper MuLV in RFV complex by addition of Ri-MuLV inhibited regression in proportion to the amount of added Ri-MuLV. These studies indicate a relationship between a change in virus tropism to NB by passage in certain hosts (e.g., Swiss/ICR mice) and the ability of Friend virus to induce erythroleukemia that spontaneously regresses. MuLV-RF isolated from the RFV complex induced lymphocytic leukemia in newborn mice which regressed and caused the regression of CFV-induced erythroleukemia. MuLV-RF is NB-tropic, contains no spleen focus-forming virus (SFFV) activity and helps SFFV form spleen foci in genetically restrictive mice. Pseudotype viruses were prepared, consisting of MuLV-RF, or other MuLV's, and SFFV derived from FV-B. The pseudotype viruses each acquired the tropism of the MuLV used in rescue. The pseudotype prepared with MuLV-RF or another NB-tropic MuLV-F, but not the virus obtained by rescue with N-tropic MuLV-F, induced erythroleukemia that spontaneously regressed. These studies demonstrate that the ability of RFV to induce erythroleukemia that spontaneously regresses is due to its helper MuLV component. |
format | Text |
id | pubmed-2180720 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1977 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21807202008-04-17 Spontaneous regression of Friend virus-induced erythroleukemia. I. The role of the helper murine leukemia virus component J Exp Med Articles The RFV strain of the Friend virus complex induces an erythroleukemia that spontaneously regresses. The tropism of regressing Friend virus complex (RFV), which is conferred by its helper MuLV component, MuLV- RF, is different from that of the conventional virus strain, CFV. RFV is NB-tropic and CFV is N-tropic. Passage of nonregressing CFV through Fv-1 incompatible Swiss/ICR mice changed the tropism of CFV from N to NB and resulted in a virus strain which induced erythroleukemia that regressed. Passage of NB-tropic CFV back through Fv-1 compatible mice maintained NB-tropism and regression. Altering the quantity or type of helper MuLV in RFV complex by addition of Ri-MuLV inhibited regression in proportion to the amount of added Ri-MuLV. These studies indicate a relationship between a change in virus tropism to NB by passage in certain hosts (e.g., Swiss/ICR mice) and the ability of Friend virus to induce erythroleukemia that spontaneously regresses. MuLV-RF isolated from the RFV complex induced lymphocytic leukemia in newborn mice which regressed and caused the regression of CFV-induced erythroleukemia. MuLV-RF is NB-tropic, contains no spleen focus-forming virus (SFFV) activity and helps SFFV form spleen foci in genetically restrictive mice. Pseudotype viruses were prepared, consisting of MuLV-RF, or other MuLV's, and SFFV derived from FV-B. The pseudotype viruses each acquired the tropism of the MuLV used in rescue. The pseudotype prepared with MuLV-RF or another NB-tropic MuLV-F, but not the virus obtained by rescue with N-tropic MuLV-F, induced erythroleukemia that spontaneously regressed. These studies demonstrate that the ability of RFV to induce erythroleukemia that spontaneously regresses is due to its helper MuLV component. The Rockefeller University Press 1977-03-01 /pmc/articles/PMC2180720/ /pubmed/233904 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Spontaneous regression of Friend virus-induced erythroleukemia. I. The role of the helper murine leukemia virus component |
title | Spontaneous regression of Friend virus-induced erythroleukemia. I. The role of the helper murine leukemia virus component |
title_full | Spontaneous regression of Friend virus-induced erythroleukemia. I. The role of the helper murine leukemia virus component |
title_fullStr | Spontaneous regression of Friend virus-induced erythroleukemia. I. The role of the helper murine leukemia virus component |
title_full_unstemmed | Spontaneous regression of Friend virus-induced erythroleukemia. I. The role of the helper murine leukemia virus component |
title_short | Spontaneous regression of Friend virus-induced erythroleukemia. I. The role of the helper murine leukemia virus component |
title_sort | spontaneous regression of friend virus-induced erythroleukemia. i. the role of the helper murine leukemia virus component |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2180720/ https://www.ncbi.nlm.nih.gov/pubmed/233904 |