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Murine and simian retrovirus models: the threshold hypothesis.

R M Ruprecht·T W Baba·R Rasmussen·Y Hu·P L Sharma
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Abstract

By considering the dynamic relationship between retroviruses and their hosts, we have developed a unifying hypothesis to explain such disparate clinical phenomena as differential pathogenicity of a given virus in adults and neonates, transient infection with clearance of provirus-containing cells, long-term non-progression and vaccine effects of fully pathogenic viruses. The threshold hypothesis predicts that an opportunity exists during acute retroviral infection to influence the ultimate clinical outcome: if virus replication is kept below threshold by any means, including drug therapy or passive immunoprophylaxis with neutralizing antibodies, the host will prevail and win the race.

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AnimalsDisease Models, AnimalDisease ProgressionHIV InfectionsHIV-1HaplorhiniHumansImmunity, CellularMiceModels, BiologicalRetroviridaeJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, Non-P.H.S.Research Support, U.S. Gov't, P.H.S.Review

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R M Ruprecht, T W Baba, R Rasmussen, Y Hu, P L Sharma. 1996. Murine and simian retrovirus models: the threshold hypothesis.. https://doi.org/10.1097/00002030-199601001-00005

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