Good evening longs.
Good news. Most important of it all is what we are going to go for in our next clinical trial:
Immune Activation is a wide-encompassing and far-reaching concept with application to a myriad of conditions. HIV produces a vicious circle where the high levels of systemic immune activation and inflammation not only promote viral replication and CD4+ T-cell apoptosis, but also promotes rapid decline of immune function and competence. The result are many diseases as Cardiovascular and Renal Diseases, Cognitive Impairment, Osteoporosis, Cancer:
https://www.hindawi.com/journals/mi/2017/6825493/
Furthermore:
The problem here is to decide which markers to look for and in what quantities to decide that there is therapeutic gain.
Maybe CD4+ CD8+ T-cell counts and ratios (markers of systemic immune activation) will be crucial and, if I don't remember wrong, we did substantial improvement in some trials on this account.
It will be very interesting to see what the protocol looks like. But, if we are successful this will be a " master key " to many conditions.
Bring it on !!!
Good news. Most important of it all is what we are going to go for in our next clinical trial:
Immune Activation is a wide-encompassing and far-reaching concept with application to a myriad of conditions. HIV produces a vicious circle where the high levels of systemic immune activation and inflammation not only promote viral replication and CD4+ T-cell apoptosis, but also promotes rapid decline of immune function and competence. The result are many diseases as Cardiovascular and Renal Diseases, Cognitive Impairment, Osteoporosis, Cancer:
https://www.hindawi.com/journals/mi/2017/6825493/
Quote:Systemic immune activation has emerged as an essential component of the immunopathogenesis of HIV. It not only leads to faster disease progression, but also to accelerated decline of overall immune competence. HIV-associated immune activation is characterized by an increase in proinflammatory mediators, dysfunctional T regulatory cells, and a pattern of T-cell-senescent phenotypes similar to those seen in the elderly. These changes predispose HIV-infected persons to comorbid conditions that have been linked to immunosenescence and inflamm-ageing, such as atherosclerosis and cardiovascular disease, neurodegeneration, and cancer. In the antiretroviral treatment era, development of such non-AIDS-defining, age-related comorbidities is a major cause of morbidity and mortality. Treatment strategies aimed at curtailing persistent immune activation and inflammation may help prevent the development of these conditions. At present, the most effective strategy appears to be early antiretroviral treatment initiation. No other treatment interventions have been found effective in large-scale clinical trials, and no adjunctive treatment is currently recommended in international HIV treatment guidelines.
Furthermore:
Quote:A number of therapeutic measures have been explored with the aim of reducing systemic immune activation in HIV-infected persons. To date, most studies have been observational in nature, making it impossible to rule out confounding factors, and to our knowledge, no human trials have used markers of immunosenescence as the primary outcome.
The problem here is to decide which markers to look for and in what quantities to decide that there is therapeutic gain.
Maybe CD4+ CD8+ T-cell counts and ratios (markers of systemic immune activation) will be crucial and, if I don't remember wrong, we did substantial improvement in some trials on this account.
It will be very interesting to see what the protocol looks like. But, if we are successful this will be a " master key " to many conditions.
Bring it on !!!
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