AIDS: caused by development of resistance to drugs in a non-target intracellular parasite.
Identifieur interne : 002136 ( PubMed/Corpus ); précédent : 002135; suivant : 002137AIDS: caused by development of resistance to drugs in a non-target intracellular parasite.
Auteurs : George E. ParrisSource :
- Medical hypotheses [ 0306-9877 ] ; 2007.
English descriptors
- KwdEn :
- Acquired Immunodeficiency Syndrome (drug therapy), Acquired Immunodeficiency Syndrome (virology), Animals, Antiviral Agents (administration & dosage), Drug Resistance, Viral, HIV (drug effects), HIV (physiology), Humans, Retroviridae (drug effects), Retroviridae (physiology), T-Lymphocytes (virology).
- MESH :
- chemical , administration & dosage : Antiviral Agents.
- drug effects : HIV, Retroviridae.
- drug therapy : Acquired Immunodeficiency Syndrome.
- physiology : HIV, Retroviridae.
- virology : Acquired Immunodeficiency Syndrome, T-Lymphocytes.
- Animals, Drug Resistance, Viral, Humans.
Abstract
The origin of acquired immune disorder syndrome (AIDS) has been the subject of substantial controversy both in the scientific community and in the popular press. The debate involves the mode of transmission of a simian virus (SIV) to humans. Both major camps in the argument presume that humans are normally free of such viruses and assume that once the simian virus was transmitted, it immediately infected some T-cells and caused the release of toxic agents that killed off bystander (uninfected) T-cells resulting in AIDS. The evolution of the Simian virus (SIV) into a human virus (HIV) is regarded as an artifact. In contrast, a fundamentally different hypothesis has been proposed [Parris GE. Med Hypotheses 2004;62(3):354-7] in which it is presumed that in hyper-endemic areas of malaria (central Africa), all primates (humans and non-human primates) have shared a retrovirus that augments their T-cell response to the malaria parasite. The virus can be called "primate T-cell retrovirus" (PTRV). Over thousands of years the virus has crossed species lines many times (with little effect) and typically adapts to the host quickly. In this model, AIDS is seen to be the result of the development of resistance of the virus (PTRV) to continuous exposure to pro-apoptotic (schizonticidal) aminoquinoline drugs used to prevent malaria. The hypothesis was originally proposed based on biochemical activities of the aminoquinolines (e.g., pamaquine (plasmoquine(TM)), primaquine and chloroquine), but recent publications demonstrated that some of these drugs definitely adversely affect HIV and other viruses and logically would cause them to evolve resistance. Review of the timeline that has been created for the evolution of HIV in humans is also shown to be qualitatively and quantitatively consistent with this hypothesis (and not with either version of the conventional hypothesis). SARS and Ebola also fit this pattern.
DOI: 10.1016/j.mehy.2006.06.011
PubMed: 16893612
Links to Exploration step
pubmed:16893612Le document en format XML
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Parris</name><affiliation><nlm:affiliation>9601 Warfield Road, Gaithersburg, MD 20882, United States. antimony_121@hotmail.com</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="RBID">pubmed:16893612</idno><idno type="pmid">16893612</idno><idno type="doi">10.1016/j.mehy.2006.06.011</idno><idno type="wicri:Area/PubMed/Corpus">002136</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002136</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">AIDS: caused by development of resistance to drugs in a non-target intracellular parasite.</title><author><name sortKey="Parris, George E" sort="Parris, George E" uniqKey="Parris G" first="George E" last="Parris">George E. Parris</name><affiliation><nlm:affiliation>9601 Warfield Road, Gaithersburg, MD 20882, United States. antimony_121@hotmail.com</nlm:affiliation></affiliation></author></analytic><series><title level="j">Medical hypotheses</title><idno type="ISSN">0306-9877</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acquired Immunodeficiency Syndrome (drug therapy)</term><term>Acquired Immunodeficiency Syndrome (virology)</term><term>Animals</term><term>Antiviral Agents (administration & dosage)</term><term>Drug Resistance, Viral</term><term>HIV (drug effects)</term><term>HIV (physiology)</term><term>Humans</term><term>Retroviridae (drug effects)</term><term>Retroviridae (physiology)</term><term>T-Lymphocytes (virology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiviral Agents</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>HIV</term><term>Retroviridae</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Acquired Immunodeficiency Syndrome</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>HIV</term><term>Retroviridae</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Acquired Immunodeficiency Syndrome</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Drug Resistance, Viral</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The origin of acquired immune disorder syndrome (AIDS) has been the subject of substantial controversy both in the scientific community and in the popular press. The debate involves the mode of transmission of a simian virus (SIV) to humans. Both major camps in the argument presume that humans are normally free of such viruses and assume that once the simian virus was transmitted, it immediately infected some T-cells and caused the release of toxic agents that killed off bystander (uninfected) T-cells resulting in AIDS. The evolution of the Simian virus (SIV) into a human virus (HIV) is regarded as an artifact. In contrast, a fundamentally different hypothesis has been proposed [Parris GE. Med Hypotheses 2004;62(3):354-7] in which it is presumed that in hyper-endemic areas of malaria (central Africa), all primates (humans and non-human primates) have shared a retrovirus that augments their T-cell response to the malaria parasite. The virus can be called "primate T-cell retrovirus" (PTRV). Over thousands of years the virus has crossed species lines many times (with little effect) and typically adapts to the host quickly. In this model, AIDS is seen to be the result of the development of resistance of the virus (PTRV) to continuous exposure to pro-apoptotic (schizonticidal) aminoquinoline drugs used to prevent malaria. The hypothesis was originally proposed based on biochemical activities of the aminoquinolines (e.g., pamaquine (plasmoquine(TM)), primaquine and chloroquine), but recent publications demonstrated that some of these drugs definitely adversely affect HIV and other viruses and logically would cause them to evolve resistance. Review of the timeline that has been created for the evolution of HIV in humans is also shown to be qualitatively and quantitatively consistent with this hypothesis (and not with either version of the conventional hypothesis). SARS and Ebola also fit this pattern.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16893612</PMID><DateCompleted><Year>2007</Year><Month>01</Month><Day>30</Day></DateCompleted><DateRevised><Year>2020</Year><Month>04</Month><Day>09</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0306-9877</ISSN><JournalIssue CitedMedium="Print"><Volume>68</Volume><Issue>1</Issue><PubDate><Year>2007</Year></PubDate></JournalIssue><Title>Medical hypotheses</Title><ISOAbbreviation>Med. Hypotheses</ISOAbbreviation></Journal><ArticleTitle>AIDS: caused by development of resistance to drugs in a non-target intracellular parasite.</ArticleTitle><Pagination><MedlinePgn>151-7</MedlinePgn></Pagination><Abstract><AbstractText>The origin of acquired immune disorder syndrome (AIDS) has been the subject of substantial controversy both in the scientific community and in the popular press. The debate involves the mode of transmission of a simian virus (SIV) to humans. Both major camps in the argument presume that humans are normally free of such viruses and assume that once the simian virus was transmitted, it immediately infected some T-cells and caused the release of toxic agents that killed off bystander (uninfected) T-cells resulting in AIDS. The evolution of the Simian virus (SIV) into a human virus (HIV) is regarded as an artifact. In contrast, a fundamentally different hypothesis has been proposed [Parris GE. Med Hypotheses 2004;62(3):354-7] in which it is presumed that in hyper-endemic areas of malaria (central Africa), all primates (humans and non-human primates) have shared a retrovirus that augments their T-cell response to the malaria parasite. The virus can be called "primate T-cell retrovirus" (PTRV). Over thousands of years the virus has crossed species lines many times (with little effect) and typically adapts to the host quickly. In this model, AIDS is seen to be the result of the development of resistance of the virus (PTRV) to continuous exposure to pro-apoptotic (schizonticidal) aminoquinoline drugs used to prevent malaria. The hypothesis was originally proposed based on biochemical activities of the aminoquinolines (e.g., pamaquine (plasmoquine(TM)), primaquine and chloroquine), but recent publications demonstrated that some of these drugs definitely adversely affect HIV and other viruses and logically would cause them to evolve resistance. Review of the timeline that has been created for the evolution of HIV in humans is also shown to be qualitatively and quantitatively consistent with this hypothesis (and not with either version of the conventional hypothesis). SARS and Ebola also fit this pattern.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Parris</LastName><ForeName>George E</ForeName><Initials>GE</Initials><AffiliationInfo><Affiliation>9601 Warfield Road, Gaithersburg, MD 20882, United States. antimony_121@hotmail.com</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2006</Year><Month>08</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Med Hypotheses</MedlineTA><NlmUniqueID>7505668</NlmUniqueID><ISSNLinking>0306-9877</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000998">Antiviral Agents</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections 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