HIV causes a chronic, persistent infection that has a latent phase.
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Another mechanism that is used to maintain the latent phase is chromatin remodeling.
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A vigorous immune response eventually controls the infection and initiates the clinically latent phase.
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Latent phase ends with the onset of active first stage, and this transition is defined retrospectively.
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Pel in 1896 supported Gogli's latent phase theory.
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Initially there is a latent phase where the wound undergoes plasma exudation, inflammatory decontamination and debridement.
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The latent phase is generally defined as beginning at the point at which the woman perceives regular uterine contractions.
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In the latent phase there is a lot of H3K9 trimethylation near the terminal repeats, which is an indication of heterochromatin in these areas.
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This means that these genes are controlled through a mechanism affecting the chromatin structure that allows them to be expressed in the latent phase.
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During the latent phase, researchers have found more methylated chromatin in the lytic genes and less acetylated chromatin, whereas in the LAT region there is less methylation and more acetylation found during latency.
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