On 2014 Dec 08, George Parris commented:

Between 2004 and 2009 I developed a hypothesis for the origin of HIV-1M based on the idea that anti-malarial drugs may have steered the evolution of HIV-1 along a unique trajectory Parris GE, 2004 Parris GE, 2007 Parris GE, 2007. My model deviates substantially from the widely accepted zoonosis model advocated by Sharp and Hahn (2008, 2011). Now, Faria et al. have independently proposed a model of HIV spread based on a detailed conventional analysis of the evolution of the HIV-1M sequence, which is consistent with my model:

Clearly the transfer of SIV to humans in SE Cameroon (about 1876 according to recent analysis Wertheim JO, 2009) substantially predates the MRCA of HIV-1M (1920s). Thus, the original SIV infection in humans lingered for as much as 50 years (1876-1926) and mutated without producing a pandemic while evolving into the HIV-1 clade. Through the 1920s many persons from SE Cameroon with HIV-1 likely visited Leopoldville (Kinshasa) via the Sangha River (see the reports of Louise Pearce concerning African sleeping sickness dating from 1921). The MRCA of HIV-1M subsequently arose in Leopoldville as a result of some unique mutations (not shared with HIV-1O or other HIV-1 groups). The date of this unique transformation has been the subject of several studies and according to Faria et al. (page 60) if subtypes B and C (which obviously evolved later) are eliminated from the dataset, the molecular clock is more appropriately calibrated and the date of the MRCA of HIV-1M settles at 1926. They point out that neither population growth nor genital ulcer disease can explain the "starburst" pattern of divergence of the numerous HIV-1M lines (i.e., few subtypes in the period 1926-1950 followed by many subtypes and sublines in the 1950s and beyond). Finally, they conclude that their findings are consistent with "iatrogenic interventions in Kinshasa...were critical for the emergence of group M." In my papers I describe a specific (well-documented) iatrogenic event in early 1927 in Leopoldville/Kinshasa, which involved a child associated by name and disease (she had sleeping sickness) with SE Cameroon and the Sangha River. It is documented that after being treated with a powerful anti-malarial (pamaquine that affects the white blood cells) she and two other young girls were tested for malaria (blood drawn by syringe) at the same place and same day in sequence.

The substantial delay in the spread of HIV-1M from Leopoldville (from 1927-1937)clarified by Faria et al. is consistent with the virus being in the bodies of children (under 10-years old in 1927). Had the virus been in the adult population (1926-onward) it undoubtedly would have spread geographically much earlier via rail and boat; moreover as a result of commercial sex workers and screening for sleeping sickness (e.g., by Jamot in Cameroon), there would have been many more unique subtypes generated in the period 1926-1940.

It is incredible to me that in spite of the fact that anti-malaria drugs (e.g., chloroquine) are known to affect the replication of HIV (see papers by Savarino A starting in 2001 Savarino A, 2001) that this effect has been universally ignored in analysis of the evolution of HIV. Chloroquine became a daily fact of life in the Congo Basin in the late 1950s, just when the starburst is observed. Moreover, suppression of HIV by chloroquine can explain why HIV was first detected in the US in the 1980s (where chloroquine was not being widely used).

On 2014 Dec 08, George Parris commented:

Between 2004 and 2009 I developed a hypothesis for the origin of HIV-1M based on the idea that anti-malarial drugs may have steered the evolution of HIV-1 along a unique trajectory Parris GE, 2004 Parris GE, 2007 Parris GE, 2007. My model deviates substantially from the widely accepted zoonosis model advocated by Sharp and Hahn (2008, 2011). Now, Faria et al. have independently proposed a model of HIV spread based on a detailed conventional analysis of the evolution of the HIV-1M sequence, which is consistent with my model:

Clearly the transfer of SIV to humans in SE Cameroon (about 1876 according to recent analysis Wertheim JO, 2009) substantially predates the MRCA of HIV-1M (1920s). Thus, the original SIV infection in humans lingered for as much as 50 years (1876-1926) and mutated without producing a pandemic while evolving into the HIV-1 clade. Through the 1920s many persons from SE Cameroon with HIV-1 likely visited Leopoldville (Kinshasa) via the Sangha River (see the reports of Louise Pearce concerning African sleeping sickness dating from 1921). The MRCA of HIV-1M subsequently arose in Leopoldville as a result of some unique mutations (not shared with HIV-1O or other HIV-1 groups). The date of this unique transformation has been the subject of several studies and according to Faria et al. (page 60) if subtypes B and C (which obviously evolved later) are eliminated from the dataset, the molecular clock is more appropriately calibrated and the date of the MRCA of HIV-1M settles at 1926. They point out that neither population growth nor genital ulcer disease can explain the "starburst" pattern of divergence of the numerous HIV-1M lines (i.e., few subtypes in the period 1926-1950 followed by many subtypes and sublines in the 1950s and beyond). Finally, they conclude that their findings are consistent with "iatrogenic interventions in Kinshasa...were critical for the emergence of group M." In my papers I describe a specific (well-documented) iatrogenic event in early 1927 in Leopoldville/Kinshasa, which involved a child associated by name and disease (she had sleeping sickness) with SE Cameroon and the Sangha River. It is documented that after being treated with a powerful anti-malarial (pamaquine that affects the white blood cells) she and two other young girls were tested for malaria (blood drawn by syringe) at the same place and same day in sequence.

The substantial delay in the spread of HIV-1M from Leopoldville (from 1927-1937)clarified by Faria et al. is consistent with the virus being in the bodies of children (under 10-years old in 1927). Had the virus been in the adult population (1926-onward) it undoubtedly would have spread geographically much earlier via rail and boat; moreover as a result of commercial sex workers and screening for sleeping sickness (e.g., by Jamot in Cameroon), there would have been many more unique subtypes generated in the period 1926-1940.

It is incredible to me that in spite of the fact that anti-malaria drugs (e.g., chloroquine) are known to affect the replication of HIV (see papers by Savarino A starting in 2001 Savarino A, 2001) that this effect has been universally ignored in analysis of the evolution of HIV. Chloroquine became a daily fact of life in the Congo Basin in the late 1950s, just when the starburst is observed. Moreover, suppression of HIV by chloroquine can explain why HIV was first detected in the US in the 1980s (where chloroquine was not being widely used).