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In a recent paper in Nature, a team led by Jeffrey Gordon, a microbiologist at Washington University, reports that each of us has, so to speak, a viral identity — a pattern of viral DNA that is highly stable and highly distinct, even among closely related humans.
Increasing evidence shows that genes have a pivotal role in affecting the dynamic pattern of viral loads in the body of a host.
To understand the pattern of viral spread, CAPRISA and the Africa Centre mapped out the infection cycle between men and women of different ages in KwaZulu-Natal.
Furthermore, the pattern of viral gene expression may be distinct from that proposed in the first hypothesis.
As represented in the three panels of Figure 3A, we can observe a pattern of viral replication throughout time for all different shRNA clones.
These results were compared to the pattern of viral evolution observed in 98 subjects during a similar phase in HIV infection from a previous study.
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Frustratingly for the federal, state and county health officials who were working to explain this ailment, it did not conform to any known patterns of viral or bacterial illness.
We observed a rapid accumulation of interhost and intrahost genetic variation, allowing us to characterize patterns of viral transmission over the initial weeks of the epidemic.
Herein, we described, for the first time, the intranuclear distribution patterns of viral DNA replication events, preceding those that occur in the cytoplasmic compartment.
Consistent with inferences based on extensive work with individual probes, the patterns of viral transcript abundance differ sufficiently in various cell types suggesting that certain aspects of viral pathogenesis must take this fact into account.
We observed similar patterns of viral production with mutant versus wild-type viral stocks than those observed by measuring p24 production in cell supernatants.
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