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Posted On: 08/09/2019 9:42:22 AM
Post# of 156888
It’s not that simple to just treat someone with leronlimab and wait 7-11 years for the viral reservoirs to die off.
For a start “undetectable” doesn’t mean there is no circulating or inactive reservoirs of virus, it just can not be detected with the current method of measurement.
Next, leronlimab needs to cover every ccr5 receptor (multi millions) consistently for this period and any new T-cells leronlimab would have to cover every receptor before the virus does.
Then when an HIV patient has say the Flu the number of T-cells increase remarkably and if there is not an increase or surplus amount of leronlimab to protect these they can get infected and possibly become a new inactive reservoir requiring an additional ~10 years.
Possibly if the hidden reservoirs and active infected cells are in small enough numbers the protected T-cells may be able to control these without the need for drugs.
Another possible solution is to High jack these infected cells back using ZFN or CRISPR.
For a start “undetectable” doesn’t mean there is no circulating or inactive reservoirs of virus, it just can not be detected with the current method of measurement.
Next, leronlimab needs to cover every ccr5 receptor (multi millions) consistently for this period and any new T-cells leronlimab would have to cover every receptor before the virus does.
Then when an HIV patient has say the Flu the number of T-cells increase remarkably and if there is not an increase or surplus amount of leronlimab to protect these they can get infected and possibly become a new inactive reservoir requiring an additional ~10 years.
Possibly if the hidden reservoirs and active infected cells are in small enough numbers the protected T-cells may be able to control these without the need for drugs.
Another possible solution is to High jack these infected cells back using ZFN or CRISPR.
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