The Puzzling Origins of AIDS]

November 19, 2004

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The Puzzling Origins of AIDS

Artist's

rendition of the HIV molecule. Credit: NIH

American Scientist -- Although no one explanation

for the origin of AIDS has been universally accepted, four rival

theories provide some important lessons.

Shortly after the 1983 discovery of the human immunodeficiency

virus (HIV), the pathogen responsible for AIDS, investigators became

aware of a strangely similar immune deficiency disease afflicting Asian

monkeys (macaques) held in captivity in various U.S. research labs.

Soon, virologists identified the culprit: a simian immunodeficiency

virus (SIV) that is found naturally in a West African monkey species,

the sooty mangabey (Cercocebus atys), but is harmless to that host.

This virus, denoted SIVsm, is genetically similar to a weakly

contagious form of the AIDS virus that is largely restricted to parts

of West Africa, HIV-2, and thus is considered its likely precursor.

More recent work has shown that the closest relative of the primary

human immunodeficiency virus (HIV- 1) is another simian

immunodeficiency virus, one carried by chimpanzees (SIVcpz).

After comparing the SIVs in chimpanzees and sooty mangabeys with

HIV-1 and HIV-2 strains, investigators concluded that there must have

been multiple transmission "events" from simians to humans-at least

seven for HIV-2 (some of which are known from only a single person who

lives near mangabeys carrying a uniquely similar SIV) and three for

HIV-1, the virus now infecting some 40 million people worldwide.

How did SIVcpz and SIVsm cross over into humans and become

pathogenic? Given the lack of historical references to AIDS-like

disease in Africa prior to the mid-20th century, as well as its absence

previously in the New World (which imported some 10 million African

slaves during the 16th through 19th centuries), that transfer appears

to have happened relatively recently-exactly when is a point of

considerable debate. And why did two distinct simian viruses with which

humans have apparently coexisted for centuries, or even millennia,

suddenly pass into humans multiple times within a few decades?

The answers to these questions have been slow in coming, despite

the considerable efforts of molecular biologists to understand the

nature and evolution of primate immunodeficiency viruses. I am not one

of those molecular biologists; rather, I became a player in the field

of AIDS-origin research through my interest in chimpanzee socioecology.

Although I am partial to a theory I helped to fashion for why AIDS

emerged when it did, with time it might become clear that a competing

idea better accounts for genesis of the epidemic. Or perhaps the answer

will prove to lie with some complex combination of factors that no

single explanation presently encompasses. Whatever the case, the

solution almost certainly will come from one or more of four competing

theories.

Theory 1: Tainted Polio Vaccine

The first theory is the most controversial. In a 1992 article in

the magazine Rolling Stone, journalist Tom Curtis suggested that HTV

could have resulted from the use in Africa of an experimental oral

polio vaccine (OPV), one contaminated by a then-unknown SIV carried

most probably (Curtis supposed) by African green monkeys. Green- monkey

kidney cells were widely used as a substrate to grow viruses for

research and vaccine production. And one of the first major trials of

an experimental oral polio virus vaccine took place from 1957 to 1960

in what are now the Democratic Republic of the Congo, Burundi and

Rwanda, seemingly the "hearth" of the global AIDS epidemic. When

interviewed by Curtis, Hilary Koprowski, the polio- vaccine pioneer who

mounted that massive campaign, could not recall or find documentary

evidence as to whether his group had used kidney cells from green

monkeys or Asian macaques (which do not naturally carry an SIV). If

culture media contained SIV (a possibility, given that the techniques

available during that era were unable to guard against unknown viruses

that did not cause overt symptoms in their monkey hosts), more than

900,000 people might have received it with their medicine, laying the

basis for the current epidemic.

Curtis credited this theory to Blaine Elswood, a Californian AIDS

activist. Interestingly, the idea that the administration of a

contaminated oral polio vaccine might have been involved in the genesis

of AIDS was suggested independently by two others at about the same

time. The first to do so was Louis Pascal, who like Elswood is not a

scientist. After years of rejections, Pascal, a New Yorker, finally

managed in 1991 to get the University of Wollongong in Australia to

publish a paper describing his ideas. Not surprisingly, few noticed it.

Attorney Walter Kyle also published a broadly similar theory in The

Lancet, a British medical journal, in 1992. Since then, writer Edward

Hooper, author of the controversial 1999 book The River, has become the

contaminated-vaccine theory's most ardent supporter. Hooper, noting a

passing mention by Curtis of a chimpanzee colony run by Koprowski's

team, suggested that kidneys from these chimpanzees-not from green

monkeys-may have been the original source of the virus.

Multiple localized strains of HIV have now been discovered, and

mass vaccination appears unlikely to account for all of them. But the

early distribution of the major pandemic strain, HIV-1 group M (for

"main"), seems to fit reasonably well with the location of Koprowski's

campaigns, and the OPV theory now is applied primarily to this strain.

Contamination of OPV is the only one of the four current theories

that is readily falsifiable: Finding the HIV-1 group M virus in a

tissue sample that predated the suspect vaccine would eliminate this

possibility. So far that has not happened. Still, many investigators

give the theory little weight for other reasons, which has led to the

widespread belief that the theory has been definitively disproved. In

2001, for example, Science magazine published a piece titled "Disputed

AIDS Theory Dies its Final Death," and Nature ran one under the heading

"Polio Vaccines Exonerated." Earlier this year Nature also published

"Origin of AIDS: Contaminated Polio Vaccine Theory Refuted"-a

surprising title given that this theory ostensibly died three years

ago.

The recent findings of various molecular biologists have indeed

failed to provide support for the OPV theory. For example, in 2000 a

few existing samples of the vaccine from Koprowski's home institution

(the Wistar Institute in Philadelphia) were tested and found negative

for both chimpanzee DNA and SIV. However, this result did not rule out

the possibility, previously suggested by Hooper, that local

amplification of the live-virus vaccine in Africa (to create more

doses) could have introduced the SIV. The key issue is thus whether

chimpanzee kidneys were used as a culture medium at any stage of

Koprowski's vaccine program. There is eyewitness testimony on both

sides of this question, and failure to find SIVcpz in a handful of

samples of the live vaccine strain of the type used in Africa does not

prove the virus was absent in (putative) locally produced batches.

A second reason to question the OPV theory also came to light in

2000, with a report in Science by Bette T. Korber (of Los Alamos

National Laboratory) and colleagues. They used molecular differences

among HIV-1 group M subtypes to estimate the date of their last common

ancestor. The conclusion: 1931 (with 95 percent confidence limits

giving the range 1915 to 1941), preceding OPV administration by

decades. However, the calculation of such common-ancestor dates can be

thrown off by genetic recombination among subtypes ("viral sex"), which

can make such dates come out too early, and there is increasing

evidence that such recombination may be common with HIV. So maybe this

date is not right. On the other hand, independent analyses using

different methods have supported the date, and an analogous study of

HIV-2 came up with an origin for the main group between 1940 and 1945.

Another objection to the OPV theory concerns the subspecies of

chimpanzee kept near Kisangani (formerly Stanleyville) at a facility

called Camp Lindi, which Koprowski and colleagues maintain was used for

safety-testing their vaccine, but which Hooper suspects was the source

of chimpanzee tissues used to produce vaccine locally. The SIVcpz

strain that is most similar to HIV-1 has so far only been identified in

a subspecies of chimpanzee native to west-central Africa, Pan

troglodytes troglodytes. A second, less similar strain has been

identified only in Pan troglodytes schweinfurthii, the subspecies found

in east-central Africa-where Camp Lindi was located. The nearest known

populations of P. t. troglodytes are more than 500 kilometers from

Koprowski's chimp colony. So, this argument goes, the locally obtained

captive chimps would not have been carrying the SIVcpz strain thought

to have given rise to HIV-1.

More- http://www.rednova.com/news/display/?id=99619#

November 21, 2004

If you are the least bit curious about what other scientists have said, visit any of these sites;

http://aras.ab.ca/

http://www.aliveandwell.org/

http://www.theperthgroup.com/

There is a whole lot more afoot here than one would expect. Notice the below "artist rendition" in lieu of an actual picture? Ask yourself why? Where is an actual picture?

S.

In a message dated 11/19/2004 9:55:31 PM Pacific Standard Time, 121 writes:

E-mail this to a friend Printable version

Change Font Size: A A A

The Puzzling Origins of AIDS

Artist's rendition of the HIV molecule. Credit: NIH

American Scientist -- Although no one explanation for the origin of AIDS has been universally accepted, four rival theories provide some important lessons.

Shortly after the 1983 discovery of the human immunodeficiency virus (HIV), the pathogen responsible for AIDS, investigators became aware of a strangely similar immune deficiency disease afflicting Asian monkeys (macaques) held in captivity in various U.S. research labs. Soon, virologists identified the culprit: a simian immunodeficiency virus (SIV) that is found naturally in a West African monkey species, the sooty mangabey (Cercocebus atys), but is harmless to that host.

This virus, denoted SIVsm, is genetically similar to a weakly contagious form of the AIDS virus that is largely restricted to parts of West Africa, HIV-2, and thus is considered its likely precursor. More recent work has shown that the closest relative of the primary human immunodeficiency virus (HIV- 1) is another simian immunodeficiency virus, one carried by chimpanzees (SIVcpz).

After comparing the SIVs in chimpanzees and sooty mangabeys with HIV-1 and HIV-2 strains, investigators concluded that there must have been multiple transmission "events" from simians to humans-at least seven for HIV-2 (some of which are known from only a single person who lives near mangabeys carrying a uniquely similar SIV) and three for HIV-1, the virus now infecting some 40 million people worldwide.

How did SIVcpz and SIVsm cross over into humans and become pathogenic? Given the lack of historical references to AIDS-like disease in Africa prior to the mid-20th century, as well as its absence previously in the New World (which imported some 10 million African slaves during the 16th through 19th centuries), that transfer appears to have happened relatively recently-exactly when is a point of considerable debate. And why did two distinct simian viruses with which humans have apparently coexisted for centuries, or even millennia, suddenly pass into humans multiple times within a few decades?

The answers to these questions have been slow in coming, despite the considerable efforts of molecular biologists to understand the nature and evolution of primate immunodeficiency viruses. I am not one of those molecular biologists; rather, I became a player in the field of AIDS-origin research through my interest in chimpanzee socioecology. Although I am partial to a theory I helped to fashion for why AIDS emerged when it did, with time it might become clear that a competing idea better accounts for genesis of the epidemic. Or perhaps the answer will prove to lie with some complex combination of factors that no single explanation presently encompasses. Whatever the case, the solution almost certainly will come from one or more of four competing theories.

Theory 1: Tainted Polio Vaccine

The first theory is the most controversial. In a 1992 article in the magazine Rolling Stone, journalist Tom Curtis suggested that HTV could have resulted from the use in Africa of an experimental oral polio vaccine (OPV), one contaminated by a then-unknown SIV carried most probably (Curtis supposed) by African green monkeys. Green- monkey kidney cells were widely used as a substrate to grow viruses for research and vaccine production. And one of the first major trials of an experimental oral polio virus vaccine took place from 1957 to 1960 in what are now the Democratic Republic of the Congo, Burundi and Rwanda, seemingly the "hearth" of the global AIDS epidemic. When interviewed by Curtis, Hilary Koprowski, the polio- vaccine pioneer who mounted that massive campaign, could not recall or find documentary evidence as to whether his group had used kidney cells from green monkeys or Asian macaques (which do not naturally carry an SIV). If culture media contained SIV (a possibility, given that the techniques available during that era were unable to guard against unknown viruses that did not cause overt symptoms in their monkey hosts), more than 900,000 people might have received it with their medicine, laying the basis for the current epidemic.

Curtis credited this theory to Blaine Elswood, a Californian AIDS activist. Interestingly, the idea that the administration of a contaminated oral polio vaccine might have been involved in the genesis of AIDS was suggested independently by two others at about the same time. The first to do so was Louis Pascal, who like Elswood is not a scientist. After years of rejections, Pascal, a New Yorker, finally managed in 1991 to get the University of Wollongong in Australia to publish a paper describing his ideas. Not surprisingly, few noticed it. Attorney Walter Kyle also published a broadly similar theory in The Lancet, a British medical journal, in 1992. Since then, writer Edward Hooper, author of the controversial 1999 book The River, has become the contaminated-vaccine theory's most ardent supporter. Hooper, noting a passing mention by Curtis of a chimpanzee colony run by Koprowski's team, suggested that kidneys from these chimpanzees-not from green monkeys-may have been the original source of the virus.

Multiple localized strains of HIV have now been discovered, and mass vaccination appears unlikely to account for all of them. But the early distribution of the major pandemic strain, HIV-1 group M (for "main"), seems to fit reasonably well with the location of Koprowski's campaigns, and the OPV theory now is applied primarily to this strain.

Contamination of OPV is the only one of the four current theories that is readily falsifiable: Finding the HIV-1 group M virus in a tissue sample that predated the suspect vaccine would eliminate this possibility. So far that has not happened. Still, many investigators give the theory little weight for other reasons, which has led to the widespread belief that the theory has been definitively disproved. In 2001, for example, Science magazine published a piece titled "Disputed AIDS Theory Dies its Final Death," and Nature ran one under the heading "Polio Vaccines Exonerated." Earlier this year Nature also published "Origin of AIDS: Contaminated Polio Vaccine Theory Refuted"-a surprising title given that this theory ostensibly died three years ago.

The recent findings of various molecular biologists have indeed failed to provide support for the OPV theory. For example, in 2000 a few existing samples of the vaccine from Koprowski's home institution (the Wistar Institute in Philadelphia) were tested and found negative for both chimpanzee DNA and SIV. However, this result did not rule out the possibility, previously suggested by Hooper, that local amplification of the live-virus vaccine in Africa (to create more doses) could have introduced the SIV. The key issue is thus whether chimpanzee kidneys were used as a culture medium at any stage of Koprowski's vaccine program. There is eyewitness testimony on both sides of this question, and failure to find SIVcpz in a handful of samples of the live vaccine strain of the type used in Africa does not prove the virus was absent in (putative) locally produced batches.

A second reason to question the OPV theory also came to light in 2000, with a report in Science by Bette T. Korber (of Los Alamos National Laboratory) and colleagues. They used molecular differences among HIV-1 group M subtypes to estimate the date of their last common ancestor. The conclusion: 1931 (with 95 percent confidence limits giving the range 1915 to 1941), preceding OPV administration by decades. However, the calculation of such common-ancestor dates can be thrown off by genetic recombination among subtypes ("viral sex"), which can make such dates come out too early, and there is increasing evidence that such recombination may be common with HIV. So maybe this date is not right. On the other hand, independent analyses using different methods have supported the date, and an analogous study of HIV-2 came up with an origin for the main group between 1940 and 1945.

Another objection to the OPV theory concerns the subspecies of chimpanzee kept near Kisangani (formerly Stanleyville) at a facility called Camp Lindi, which Koprowski and colleagues maintain was used for safety-testing their vaccine, but which Hooper suspects was the source of chimpanzee tissues used to produce vaccine locally. The SIVcpz strain that is most similar to HIV-1 has so far only been identified in a subspecies of chimpanzee native to west-central Africa, Pan troglodytes troglodytes. A second, less similar strain has been identified only in Pan troglodytes schweinfurthii, the subspecies found in east-central Africa-where Camp Lindi was located. The nearest known populations of P. t. troglodytes are more than 500 kilometers from Koprowski's chimp colony. So, this argument goes, the locally obtained captive chimps would not have been carrying the SIVcpz strain thought to have given rise to HIV-1.

More- http://www.rednova.com/news/display/?id=99619#

November 21, 2004

- lenfesteys

Sunday, November 21, 2004 2:15 AM

Re: The Puzzling Origins of AIDS]

If you are the least bit curious about what other scientists have said, visit any of these sites;

http://aras.ab.ca/

http://www.aliveandwell.org/

http://www.theperthgroup.com/

There is a whole lot more afoot here than one would expect. Notice the below "artist rendition" in lieu of an actual picture? Ask yourself why? Where is an actual picture?

S.

In a message dated 11/19/2004 9:55:31 PM Pacific Standard Time, 121 writes:

E-mail this to a friend Printable version

Change Font Size: A A A

The Puzzling Origins of AIDS

Artist's rendition of the HIV molecule. Credit: NIH

American Scientist -- Although no one explanation for the origin of AIDS has been universally accepted, four rival theories provide some important lessons.

Shortly after the 1983 discovery of the human immunodeficiency virus (HIV), the pathogen responsible for AIDS, investigators became aware of a strangely similar immune deficiency disease afflicting Asian monkeys (macaques) held in captivity in various U.S. research labs. Soon, virologists identified the culprit: a simian immunodeficiency virus (SIV) that is found naturally in a West African monkey species, the sooty mangabey (Cercocebus atys), but is harmless to that host.

This virus, denoted SIVsm, is genetically similar to a weakly contagious form of the AIDS virus that is largely restricted to parts of West Africa, HIV-2, and thus is considered its likely precursor. More recent work has shown that the closest relative of the primary human immunodeficiency virus (HIV- 1) is another simian immunodeficiency virus, one carried by chimpanzees (SIVcpz).

After comparing the SIVs in chimpanzees and sooty mangabeys with HIV-1 and HIV-2 strains, investigators concluded that there must have been multiple transmission "events" from simians to humans-at least seven for HIV-2 (some of which are known from only a single person who lives near mangabeys carrying a uniquely similar SIV) and three for HIV-1, the virus now infecting some 40 million people worldwide.

How did SIVcpz and SIVsm cross over into humans and become pathogenic? Given the lack of historical references to AIDS-like disease in Africa prior to the mid-20th century, as well as its absence previously in the New World (which imported some 10 million African slaves during the 16th through 19th centuries), that transfer appears to have happened relatively recently-exactly when is a point of considerable debate. And why did two distinct simian viruses with which humans have apparently coexisted for centuries, or even millennia, suddenly pass into humans multiple times within a few decades?

The answers to these questions have been slow in coming, despite the considerable efforts of molecular biologists to understand the nature and evolution of primate immunodeficiency viruses. I am not one of those molecular biologists; rather, I became a player in the field of AIDS-origin research through my interest in chimpanzee socioecology. Although I am partial to a theory I helped to fashion for why AIDS emerged when it did, with time it might become clear that a competing idea better accounts for genesis of the epidemic. Or perhaps the answer will prove to lie with some complex combination of factors that no single explanation presently encompasses. Whatever the case, the solution almost certainly will come from one or more of four competing theories.

Theory 1: Tainted Polio Vaccine

The first theory is the most controversial. In a 1992 article in the magazine Rolling Stone, journalist Tom Curtis suggested that HTV could have resulted from the use in Africa of an experimental oral polio vaccine (OPV), one contaminated by a then-unknown SIV carried most probably (Curtis supposed) by African green monkeys. Green- monkey kidney cells were widely used as a substrate to grow viruses for research and vaccine production. And one of the first major trials of an experimental oral polio virus vaccine took place from 1957 to 1960 in what are now the Democratic Republic of the Congo, Burundi and Rwanda, seemingly the "hearth" of the global AIDS epidemic. When interviewed by Curtis, Hilary Koprowski, the polio- vaccine pioneer who mounted that massive campaign, could not recall or find documentary evidence as to whether his group had used kidney cells from green monkeys or Asian macaques (which do not naturally carry an SIV). If culture media contained SIV (a possibility, given that the techniques available during that era were unable to guard against unknown viruses that did not cause overt symptoms in their monkey hosts), more than 900,000 people might have received it with their medicine, laying the basis for the current epidemic.

Curtis credited this theory to Blaine Elswood, a Californian AIDS activist. Interestingly, the idea that the administration of a contaminated oral polio vaccine might have been involved in the genesis of AIDS was suggested independently by two others at about the same time. The first to do so was Louis Pascal, who like Elswood is not a scientist. After years of rejections, Pascal, a New Yorker, finally managed in 1991 to get the University of Wollongong in Australia to publish a paper describing his ideas. Not surprisingly, few noticed it. Attorney Walter Kyle also published a broadly similar theory in The Lancet, a British medical journal, in 1992. Since then, writer Edward Hooper, author of the controversial 1999 book The River, has become the contaminated-vaccine theory's most ardent supporter. Hooper, noting a passing mention by Curtis of a chimpanzee colony run by Koprowski's team, suggested that kidneys from these chimpanzees-not from green monkeys-may have been the original source of the virus.

Multiple localized strains of HIV have now been discovered, and mass vaccination appears unlikely to account for all of them. But the early distribution of the major pandemic strain, HIV-1 group M (for "main"), seems to fit reasonably well with the location of Koprowski's campaigns, and the OPV theory now is applied primarily to this strain.

Contamination of OPV is the only one of the four current theories that is readily falsifiable: Finding the HIV-1 group M virus in a tissue sample that predated the suspect vaccine would eliminate this possibility. So far that has not happened. Still, many investigators give the theory little weight for other reasons, which has led to the widespread belief that the theory has been definitively disproved. In 2001, for example, Science magazine published a piece titled "Disputed AIDS Theory Dies its Final Death," and Nature ran one under the heading "Polio Vaccines Exonerated." Earlier this year Nature also published "Origin of AIDS: Contaminated Polio Vaccine Theory Refuted"-a surprising title given that this theory ostensibly died three years ago.

The recent findings of various molecular biologists have indeed failed to provide support for the OPV theory. For example, in 2000 a few existing samples of the vaccine from Koprowski's home institution (the Wistar Institute in Philadelphia) were tested and found negative for both chimpanzee DNA and SIV. However, this result did not rule out the possibility, previously suggested by Hooper, that local amplification of the live-virus vaccine in Africa (to create more doses) could have introduced the SIV. The key issue is thus whether chimpanzee kidneys were used as a culture medium at any stage of Koprowski's vaccine program. There is eyewitness testimony on both sides of this question, and failure to find SIVcpz in a handful of samples of the live vaccine strain of the type used in Africa does not prove the virus was absent in (putative) locally produced batches.

A second reason to question the OPV theory also came to light in 2000, with a report in Science by Bette T. Korber (of Los Alamos National Laboratory) and colleagues. They used molecular differences among HIV-1 group M subtypes to estimate the date of their last common ancestor. The conclusion: 1931 (with 95 percent confidence limits giving the range 1915 to 1941), preceding OPV administration by decades. However, the calculation of such common-ancestor dates can be thrown off by genetic recombination among subtypes ("viral sex"), which can make such dates come out too early, and there is increasing evidence that such recombination may be common with HIV. So maybe this date is not right. On the other hand, independent analyses using different methods have supported the date, and an analogous study of HIV-2 came up with an origin for the main group between 1940 and 1945.

Another objection to the OPV theory concerns the subspecies of chimpanzee kept near Kisangani (formerly Stanleyville) at a facility called Camp Lindi, which Koprowski and colleagues maintain was used for safety-testing their vaccine, but which Hooper suspects was the source of chimpanzee tissues used to produce vaccine locally. The SIVcpz strain that is most similar to HIV-1 has so far only been identified in a subspecies of chimpanzee native to west-central Africa, Pan troglodytes troglodytes. A second, less similar strain has been identified only in Pan troglodytes schweinfurthii, the subspecies found in east-central Africa-where Camp Lindi was located. The nearest known populations of P. t. troglodytes are more than 500 kilometers from Koprowski's chimp colony. So, this argument goes, the locally obtained captive chimps would not have been carrying the SIVcpz strain thought to have given rise to HIV-1.

More- http://www.rednova.com/news/display/?id=99619#

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