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Viral persistence depends on the balance between viral replication and host immune responses.
Live chikungunya vaccines have been abandoned to avoid the possible risk of viral persistence [77].
However, poor immunity results in viral persistence, chronic inflammation and finally liver cirrhosis and carcinoma.
Viral persistence is thought to be related to poor HBV-specific T-cell responses.
One drawback to their use is the potential for recombination and viral persistence.
Gene therapy exploits these viral persistence strategies to achieve efficient and safe long-term transgene expression.
A high incidence of viral persistence and progression to chronic hepatitis are characteristic features of hepatitis C virus (HCV) infection.
The genomic diversity of high-risk human papillomaviruses (HPV) has been associated with viral persistence and HPV-induced lesions.
Where HIV integrates into the host genome contributes to viral persistence and the expansion of infected cells.
Viral persistence in normal testis, germ cell aplasia tissues, or hepatic/splenic tissues was not observed in this study.
Readthrough transcription of the host gene might therefore suppress HIV-1 gene expression and promote the latent infection that allows viral persistence in patients on therapy.
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