Related Experiment Video
Updated: Aug 3, 2026
07:10
Humanized NOD/SCID/IL2rγnull (hu-NSG) Mouse Model for HIV Replication and Latency Studies
Published on: January 7, 2019
Murine and simian retrovirus models: the threshold hypothesis
R M Ruprecht1, T W Baba, R Rasmussen
1Laboratory of Viral Pathogenesis, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
AIDS (London, England)
|January 1, 1996
Summary
A new threshold hypothesis explains retroviral infection outcomes. Keeping virus replication low during acute infection, through therapies or antibodies, allows the host to overcome the virus.
Area of Science:
- * Virology and immunology
- * Host-pathogen dynamics
Background:
- * Retroviral infections exhibit diverse clinical outcomes, including varying pathogenicity, transient infections, and long-term non-progression.
- * The mechanisms underlying these different clinical trajectories remain incompletely understood.
Purpose of the Study:
- * To propose a unifying hypothesis explaining the varied clinical manifestations of retroviral infections.
- * To identify a critical window during acute infection that influences long-term disease progression.
Main Methods:
- * Theoretical modeling based on the dynamic interplay between retroviruses and host immune responses.
- * Analysis of existing clinical and experimental data on retroviral infections.
Main Results:
- * The threshold hypothesis posits that controlling early viral replication is key to determining clinical outcome.
- * Maintaining viral load below a critical threshold can lead to host control and viral clearance.
- * Interventions such as antiviral drugs or passive antibody administration can lower this threshold.
Conclusions:
- * Acute retroviral infection presents a critical opportunity to influence the host's ability to control the virus.
- * The threshold hypothesis provides a framework for understanding differential pathogenicity and vaccine efficacy.
- * Early and effective control of viral replication is crucial for achieving a favorable clinical outcome in retroviral infections.
Related Concept Videos
01:10Retrovirus Life Cycles
Retroviruses have a single-stranded RNA genome that undergoes a special form of replication. Once the retrovirus has entered the host cell, an enzyme called reverse transcriptase synthesizes double-stranded DNA from the retroviral RNA genome. This DNA copy of the genome is then integrated into the host’s genome inside the nucleus via an enzyme called integrase. Consequently, the retroviral genome is transcribed into RNA whenever the host’s genome is transcribed, allowing the retrovirus to...
01:51Mechanisms of Retrovirus-induced Cancers
Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
02:43Mouse Models of Cancer Study
Mice have long served as models for studying human biology and pathology because of their phylogenetic and physiological similarity with humans. They are also easy to maintain and breed in the laboratory, and hence, many inbred strains are now available for research. Studies on mice have contributed immeasurably to our understanding of cancer biology.
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...
The development of transgenic, knockout, and knock-in mice has led to an exponential increase in their use as model organisms in research,...