What's Included With Every Purchase?
You will get tested for CCR5-Delta32. CCR5-delta32 is a deletion mutation of a gene and only 1% of the total population has two copies of this gene. Individuals who carry two copies of this genetic mutation are immune to Smallpox, The Bubonic Plague (Black Death) and are also resistant to HIV, the virus that causes AIDS. Up to 20% of the population carry only one copy of this genetic mutation depending on your background and although they still run a significant risk of contracting HIV, the progress of the disease is greatly reduced and can result in a longer life expectancy. For further information please look for (CCR5-Delta32) under the Research Tab.
You will get tested for APOBEC3G protein production. In a small number of people, one in every 300 infected with HIV, the virus is naturally suppressed without medical treatment due to APOBEC3G. These people may carry high quantities of a protein APOBEC3G that disrupts viral replication in cells. APOBEC3G, or "A3" for short, is a protein that sabotages reverse transcription, the process HIV relies on for its replication. This process involves the virus transcribing its single-stranded RNA genome into double-stranded DNA that is incorporated into the cell's genome. A3 usually stops dormant viruses in the human genome, called endogenous retroviruses, from reawakening and causing infections. For further information please look for (APOBEC3G) under the Research Tab.
You will get tested for HLA-B57 and HLA-B27. Healthy individuals with HLA-B27 and HLA-B57 alleles who get infected with HIV-1 commonly remain healthy for decades without antiretroviral therapy. About 3 percent of the general population has HLA-B27 and HLA-B57. Individuals expressing the protective alleles HLA-B57 or HLA-B27 were both found to elicit immune responses against regions of the Hepatitis C Virus (HCV) polymerase protein that are critical to the ability of the virus to replicate. These immune responses force the virus to develop highly deleterious escape mutations that significantly impair virus replication, even resulting in the development of secondary ‘compensatory’ mutations by the virus in anattempt to minimize the effects of these escaped mutations. Importantly, HLA-B57 and HLA-B27 function to control HIV through a similar mechanism of selecting for highly deleterious mutations in critical regions of HIV. For further information please look for (HLA-B57 and HLA-B27) under the Research Tab.
You will get tested for DRB1*13 and DQB1*6. These genes have been linked to HIV-positive individuals called nonprogressors, who do not progress to AIDS despite lack of treatment. Researchers have broadened our understanding of this phenomenon with their finding that those lucky enough to possess both DRB1*13 and DQB1*6 have T cells with super-strength in recognizing HIV. If ever infected with HIV; healthy individuals who carry both DRB1*13 and DQB1*6 genes and are not taking antiretroviral therapy (ART) are able to maintain low viral loads and near normal CD4 T-cell counts. Researchers also concluded that the preservation and expansion of both HIV-specific CD4 and CD8 T cells may be key mechanisms by which HIV controllers keep their virus in check. For further information please look for (DRB1*13 and DQB1*6) under the Research Tab.
You will get tested for MTHFR(C677T, A1298C). MTHFR (C677T, A1298C) have been associated with a variety of multifactorial disorders like Neural Tube Defects, vascular disorders, Down syndrome, osteoporosis, bad obstetric history, cardiovascular issues and male infertility. There are over 50 variants of MTHFR, it is most commonly broken down into either C677t or A1298. The C667t variation is more commonly associated with heart disease and stroke, while the A1298 variation is most commonly associated with chronic illnesses. For further information please look for (MTHFR(C677T, A1298C)) under the Research Tab.