This entire blog post was inspired by the science article *doi:10.1016/j.ebiom.2015.01.015.* I have previously written a blog about HIV conspiracy theories, and this article does a good job at linking at providing proof concerning a few of the facts. Although the patient numbers are fairly few and specific so I won’t be about to use it as proof.
*Additional HIV transmission in those who don’t use protection which allows recombinant HIV strains to mix.
*Opportunistic infections seen in healthy individuals where the organism itself would not cause disease.
*Differing onset times indicate the preventative drugs themselves are not the sole cause of illness.
CRF19_cpx is an Evolutionary fit HIV-1 Variant Strongly Associated With Rapid Progression to AIDS in Cuba
I will start with the Study Population. Everyone that this research uses to gain data are HIV-1 positive patients that are currently at the hospital being treated for medical care. This narrows the pool of information to those most at risk to the virus.
There is no HIV-1 negative “control” patients. It appears as their control is people who have the HIV virus and those that have HIV-1 but are classified as “non-AIDS.” This *negative* control would not only have provided information to debunk conspiracy theorists, but would have also indicated that the process used to find particulates such as the following are accurate.
****Log VL at sampling (RNA copies/ml plasma) 3.7 (3.0–4.3) (N = 20) 4.7 (4.2–5.4) (N = 22) 4.7 (4.0–5.4) (N = 47) 0.0028 N0.99 0.0033****
I do applaud this study because ethey do give an effort to include the RNA copies/ml (assumed to be HIV RNA copies) rather than just taking a look at the viral load on the system (interleukins, inflamatory cytokines, ect.
5 out of the 9 patients exhibiting CRF_19 have oral candidiasis. They also were less likely to use any type of protection indicating the likelyhood of contracting multiple strains of HIV. (Which creates the CRF recombination). I would like to know if these 9 patients at all were intimate with each other.
C. albicans is carried in the mouths of about 50% of the world’s population as a normal component of the oral microbiota (wikipedia). As an opportunistic infection from a microbe that is already present, it gives greater strength to the belief that HIV is the cause of the illness.
I tried to find out how they subtype HIV, and for the most part they do use envelope proteins. This type of system is acceptable, and I may myself replace the charts listed elsewhere that provide the reasoning as:
Subtype A: Central and East Africa as well as East European countries that were formerly part of the Soviet Union.
Subtype B: West and Central Europe, the Americas, Australia, South America, and several southeast Asian countries (Thailand, and Japan), as well as northern Africa and the Middle East.
Subtype C: Sub-Saharan Africa, India, and Brazil.
Subtype D: North Africa and the Middle East.
Subtype F: South and southeast Asia.
Subtype G: West and Central Africa.
Subtypes H, J, and K: Africa and the Middle East.
A few faccts about CRF19 itself:
CRF stands for Circulating Recombinant Forms
CRF19 is a recombinant of subtype D (C-part of Gag, PR, RT and nef), subtype A (N-part of Gag, Integrase, Env) and subtype G (Vif, Vpr, Vpu and C-part of Env).
CRF19’s onset of AIDS is likely triggered by the use of RANTES and an extra effecient protease. RANTES is a part of our host system and acts by binding to CCR5. HIV utilizes CCR5 in end stages to progress, and previously this stage is what slowed down AIDS progression. Protease is a part of subtype D HIV strains, and this enzyme allows the viral proteins to form mature virons fasters.