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Báo cáo y học: It's the virus, stupid – part 2
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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài:Its the virus, stupid – part 2
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Báo cáo y học: " Its the virus, stupid – part 2"Retrovirology BioMed Central Open AccessEditorialIts the virus, stupid – part 2Ben Berkhout*Address: Department of Human Retrovirology, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsEmail: Ben Berkhout* - b.berkhout@amc.uva.nl* Corresponding authorPublished: 16 December 2005 Received: 15 December 2005 Accepted: 16 December 2005Retrovirology 2005, 2:78 doi:10.1186/1742-4690-2-78This article is available from: http://www.retrovirology.com/content/2/1/78© 2005 Berkhout; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract This editorial presents Retrovirologys choice for the best basic science retrovirus paper of the year 2005.Chronic HIV-1 infection is characterized by a steady but old message Its the virus, stupid – part 2. I find that twogenerally slow loss of CD4+ T cells. A central puzzle of of the best basic science retrovirus papers of 2005 are theHIV-1 research in the early 90s has been how the virus works from Joseph Mattapallil and colleagues and Ging-could cause AIDS, when it infects a trivial number of T sheng Li and colleagues describing that HIV-1 infects and kills the memory CD4+T cells, a T-cell subset responsiblecells. It took until 1995 before it was realized that massivevirus replication occurs during chronic infection [1]. A for remembering previous infections [2], [3]. This initialmodel was proposed in which HIV-1 kills healthy cells assault may determine the outcome of the lengthy battleslightly faster than the human body is able to replenish. between SIV-HIV and its host.David Ho, in a paraphrase of former US president BillClinton, said Its the virus, stupid to underscore the pri- Mattapallil et al. used a technique that can detect a singlemary role of the virus in the pathogenesis of AIDS. This copy of SIV DNA to show that 30–60% of all memory CD4+ T cells were infected within 10 days of viral chal-finding sets the stage for the implementation of viral loadtests in routine diagnostics. The new concept also pro- lenge. Most of these cells in the infected rhesus macaquevided the rationale for attempts to block the furiously rep- had disappeared 4 days later. There is an exclusive loss of memory CD4+T cells not only from gut-associatedlicating virus with antivirals, instead of resolving thedisease by modulating the immune system. mucosal tissues, but also from organized lymph nodes and peripheral blood. Li et al. characterized the activationNevertheless, the frequency of infected peripheral CD4+ T status of the SIV-producing cells in tissue sections, whichcells in the chronic phase of HIV-1 infection is too low turn out to be predominantly resting lymphocytes. This(0.01 – 1%) to account for the ongoing depletion of these result may be surprising because this virus is known tocells by viral infection. In addition, the mechanism for the replicate more efficiently in activated cells, but mucosalmassive and rapid loss during the acute phase of infection lymphocytes are probably better described as recentlyremains unknown. Recent work with HIV-1 and SIV in the activated. Mattapallil suggests that the high rate of infec-macaque model demonstrated that acute infection is tion of these cells is a sufficient mechanism to account foraccompanied by a dramatic and selective loss of memory their loss during acute infection; no bystander mecha-CD4+ T cells predominantly from the mucosal surfaces, ...
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Báo cáo y học: " Its the virus, stupid – part 2"Retrovirology BioMed Central Open AccessEditorialIts the virus, stupid – part 2Ben Berkhout*Address: Department of Human Retrovirology, Academic Medical Center, University of Amsterdam, Amsterdam, The NetherlandsEmail: Ben Berkhout* - b.berkhout@amc.uva.nl* Corresponding authorPublished: 16 December 2005 Received: 15 December 2005 Accepted: 16 December 2005Retrovirology 2005, 2:78 doi:10.1186/1742-4690-2-78This article is available from: http://www.retrovirology.com/content/2/1/78© 2005 Berkhout; licensee BioMed Central Ltd.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0),which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract This editorial presents Retrovirologys choice for the best basic science retrovirus paper of the year 2005.Chronic HIV-1 infection is characterized by a steady but old message Its the virus, stupid – part 2. I find that twogenerally slow loss of CD4+ T cells. A central puzzle of of the best basic science retrovirus papers of 2005 are theHIV-1 research in the early 90s has been how the virus works from Joseph Mattapallil and colleagues and Ging-could cause AIDS, when it infects a trivial number of T sheng Li and colleagues describing that HIV-1 infects and kills the memory CD4+T cells, a T-cell subset responsiblecells. It took until 1995 before it was realized that massivevirus replication occurs during chronic infection [1]. A for remembering previous infections [2], [3]. This initialmodel was proposed in which HIV-1 kills healthy cells assault may determine the outcome of the lengthy battleslightly faster than the human body is able to replenish. between SIV-HIV and its host.David Ho, in a paraphrase of former US president BillClinton, said Its the virus, stupid to underscore the pri- Mattapallil et al. used a technique that can detect a singlemary role of the virus in the pathogenesis of AIDS. This copy of SIV DNA to show that 30–60% of all memory CD4+ T cells were infected within 10 days of viral chal-finding sets the stage for the implementation of viral loadtests in routine diagnostics. The new concept also pro- lenge. Most of these cells in the infected rhesus macaquevided the rationale for attempts to block the furiously rep- had disappeared 4 days later. There is an exclusive loss of memory CD4+T cells not only from gut-associatedlicating virus with antivirals, instead of resolving thedisease by modulating the immune system. mucosal tissues, but also from organized lymph nodes and peripheral blood. Li et al. characterized the activationNevertheless, the frequency of infected peripheral CD4+ T status of the SIV-producing cells in tissue sections, whichcells in the chronic phase of HIV-1 infection is too low turn out to be predominantly resting lymphocytes. This(0.01 – 1%) to account for the ongoing depletion of these result may be surprising because this virus is known tocells by viral infection. In addition, the mechanism for the replicate more efficiently in activated cells, but mucosalmassive and rapid loss during the acute phase of infection lymphocytes are probably better described as recentlyremains unknown. Recent work with HIV-1 and SIV in the activated. Mattapallil suggests that the high rate of infec-macaque model demonstrated that acute infection is tion of these cells is a sufficient mechanism to account foraccompanied by a dramatic and selective loss of memory their loss during acute infection; no bystander mecha-CD4+ T cells predominantly from the mucosal surfaces, ...
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