PLoS Articles

User Collection Public
UNC logo

UNC-authored articles published by the Public Library of Science (PLoS)

Works (2111)

View results as:
List List Masonry Masonry Slideshow Slideshow
Sort the listing of items  

1741. A trip down memory lane with Retrovirology

Title Tesim:
A trip down memory lane with Retrovirology
Creator:
Nijhuis, Monique, Venter, Francois, Garcia-Martinez, J. Victor, Strebel, Klaus, Ross, Susan, Mak, Johnson, Fujii, Masahiro, Kirchhoff, Frank, Fassati, Ariberto, Benkirane, Monsef, Parent, Leslie, Berkhout, Ben, Margolis, D., Lever, Andrew, and Borrow, Persephone
Date of publication:
2020
Abstract Tesim:
Fifteen years ago, Retrovirology was amongst the first open-access journals to be established through Biomed Central, instigated by our late Founding Editor Dr. Kuan- Teh Jeang. Since then, in what seemed like a rather daring move to be paper-free, Retrovirology has witnessed the exponential growth of open access journals that have changed the landscape of scientific publishing and communications. As was pointed out by the staff editors in PLoS Biology [1], the infancy of open access journal was a very different time from our present day, which was before smartphones, prior to most of the digital social media platforms and at a time when we had only begun to learn about the completed DNA sequences from the Human Genome Project.
Resource type:
Article
Affiliation Label Tesim:
University of North Carolina at Chapel Hill
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/4ysg-bq28
ISSN:
1742-4690
Journal Issue:
1
Journal Title:
Retrovirology
Journal Volume:
16
Keyword:
awards and prizes, cyclophilin A, nonhuman, Retroviridae, T lymphocyte, Human immunodeficiency virus infection, Review, retrovirology, microRNA, Xenotropic murine leukemia virus, human, virology, and virus capsid
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
Person:
Nijhuis, Monique, Venter, Francois, Garcia-Martinez, J. Victor, Strebel, Klaus, Ross, Susan, Mak, Johnson, Fujii, Masahiro, Kirchhoff, Frank, Fassati, Ariberto, Benkirane, Monsef, Parent, Leslie, Berkhout, Ben, Margolis, D., Lever, Andrew, and Borrow, Persephone
Rights Statement Label:
In Copyright
Source:
79408355v

1742. Human breast milk and antiretrovirals dramatically reduce oral HIV-1 transmission in BLT humanized mice

Title Tesim:
Human breast milk and antiretrovirals dramatically reduce oral HIV-1 transmission in BLT humanized mice
Creator:
Chateau, Morgan, Denton, Paul W., Garcia, J. Victor, Swanson, Michael D., Wahl, Angela, Nochi, Tomonori, and Olesen, Rikke
Date of publication:
2012
Abstract Tesim:
Currently, over 15% of new HIV infections occur in children. Breastfeeding is a major contributor to HIV infections in infants. This represents a major paradox in the field because in vitro, breast milk has been shown to have a strong inhibitory effect on HIV infectivity. However, this inhibitory effect has never been demonstrated in vivo. Here, we address this important paradox using the first humanized mouse model of oral HIV transmission. We established that reconstitution of the oral cavity and upper gastrointestinal (GI) tract of humanized bone marrow/liver/thymus (BLT) mice with human leukocytes, including the human cell types important for mucosal HIV transmission (i.e. dendritic cells, macrophages and CD4+ T cells), renders them susceptible to oral transmission of cell-free and cell-associated HIV. Oral transmission of HIV resulted in systemic infection of lymphoid and non-lymphoid tissues that is characterized by the presence of HIV RNA in plasma and a gradual decline of CD4+ T cells in peripheral blood. Consistent with infection of the oral cavity, we observed virus shedding into saliva. We then evaluated the role of human breast milk on oral HIV transmission. Our in vivo results demonstrate that breast milk has a strong inhibitory effect on oral transmission of both cell-free and cell-associated HIV. Finally, we evaluated the effect of antiretrovirals on oral transmission of HIV. Our results show that systemic antiretrovirals administered prior to exposure can efficiently prevent oral HIV transmission in BLT mice.
Resource type:
Article
Affiliation Label Tesim:
Center for AIDS Research
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/34a9-y417
Identifier:
https://dx.doi.org/10.1371/journal.ppat.1002732
ISSN:
1553-7366
Journal Issue:
6
Journal Title:
PLoS Pathogens
Journal Volume:
8
Keyword:
virus transmission, animal experiment, breast milk, drug effect, infection prevention, antiretrovirus agent; ; ; article; ; ; ; ; , rat strain, Human immunodeficiency virus 1 infection , mouse, nonhuman, controlled study, Human immunodeficiency virus 1, virus inhibition, drug efficacy, treatment outcome, and animal model
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
Person:
Chateau, Morgan, Denton, Paul W., Garcia, J. Victor, Swanson, Michael D., Wahl, Angela, Nochi, Tomonori, and Olesen, Rikke
Rights Statement Label:
In Copyright
Source:
0p096d11n

1743. Hypogammaglobulinemia in BLT humanized mice - An animal model of primary antibody deficiency

Title Tesim:
Hypogammaglobulinemia in BLT humanized mice - An animal model of primary antibody deficiency
Creator:
Martinez-Torres, Francisco, Garcia, J. Victor, Wahl, Angela, Nochi, Tomonori, and Denton, Paul W.
Date of publication:
2014
Abstract Tesim:
Primary antibody deficiencies present clinically as reduced or absent plasma antibodies without another identified disorder that could explain the low immunoglobulin levels. Bone marrow-liver-thymus (BLT) humanized mice also exhibit primary antibody deficiency or hypogammaglobulinemia. Comprehensive characterization of B cell development and differentiation in BLT mice revealed other key parallels with primary immunodeficiency patients. We found that B cell ontogeny was normal in the bone marrow of BLT mice but observed an absence of switched memory B cells in the periphery. PC-KLH immunizations led to the presence of switched memory B cells in immunized BLT mice although plasma cells producing PC-or KLH-specific IgG were not detected in tissues. Overall, we have identified the following parallels between the humoral immune systems of primary antibody deficiency patients and those in BLT mice that make this in vivo model a robust and translational experimental platform for gaining a greater understanding of this heterogeneous array of humoral immunodeficiency disorders in humans: (i) hypogammaglobulinemia; (ii) normal B cell ontogeny in bone marrow; and (iii) poor antigen-specific IgG response to immunization. Furthermore, the development of strategies to overcome these humoral immune aberrations in BLT mice may in turn provide insights into the pathogenesis of some primary antibody deficiency patients which could lead to novel clinical interventions for improved humoral immune function.
Resource type:
Article
Affiliation Label Tesim:
Center for AIDS Research
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/v3kq-1x39
Identifier:
https://dx.doi.org/10.1371/journal.pone.0108663
ISSN:
1932-6203
Journal Issue:
10
Journal Title:
PLoS ONE
Journal Volume:
9
Keyword:
CD19 antigen, immunoglobulin G, immunoglobulin A, CD27 antigen, keyhole limpet hemocyanin, CD38 antigen, CD45 antigen, immunoglobulin M, phosphorylcholine, and immunoglobulin D
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
Person:
Martinez-Torres, Francisco, Garcia, J. Victor, Wahl, Angela, Nochi, Tomonori, and Denton, Paul W.
Rights Statement Label:
In Copyright
Source:
fq978079b

1744. Fidelity Variants of RNA Dependent RNA Polymerases Uncover an Indirect, Mutagenic Activity of Amiloride Compounds

Title Tesim:
Fidelity Variants of RNA Dependent RNA Polymerases Uncover an Indirect, Mutagenic Activity of Amiloride Compounds
Creator:
Arnold, Jamie J., Gnädig, Nina F., Vignuzzi, Marco, McPherson, Malia j., Beaucourt, Stephanie, Baron, Bruno, and Levi, Laura I.
Date of publication:
2010
Abstract Tesim:
In a screen for RNA mutagen resistance, we isolated a high fidelity RNA dependent RNA polymerase (RdRp) variant of Coxsackie virus B3 (CVB3). Curiously, this variant A372V is also resistant to amiloride. We hypothesize that amiloride has a previously undescribed mutagenic activity. Indeed, amiloride compounds increase the mutation frequencies of CVB3 and poliovirus and high fidelity variants of both viruses are more resistant to this effect. We hypothesize that this mutagenic activity is mediated through alterations in intracellular ions such as Mg2+ and Mn2+, which in turn increase virus mutation frequency by affecting RdRp fidelity. Furthermore, we show that another amiloride-resistant RdRp variant, S299T, is completely resistant to this mutagenic activity and unaffected by changes in ion concentrations. We show that RdRp variants resist the mutagenic activity of amiloride via two different mechanisms: 1) increased fidelity that generates virus populations presenting lower basal mutation frequencies or 2) resisting changes in divalent cation concentrations that affect polymerase fidelity. Our results uncover a new antiviral approach based on mutagenesis.
Resource type:
Article
Affiliation Label Tesim:
Department of Microbiology and Immunology
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/ctn8-qn82
Identifier:
https://dx.doi.org/10.1371/journal.ppat.1001163
ISSN:
1553-7366
Journal Issue:
10
Journal Title:
PLoS Pathogens
Journal Volume:
6
Keyword:
amiloride, magnesium, RNA directed RNA polymerase, ion, manganese, and mutagenic agent
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
Pennsylvania State University and Institut Pasteur
Person:
Arnold, Jamie J., Gnädig, Nina F., Vignuzzi, Marco, McPherson, Malia j., Beaucourt, Stephanie, Baron, Bruno, and Levi, Laura I.
Rights Statement Label:
In Copyright
Source:
2n49t7360

1745. LIGHT induces distinct signals to clear an AAVexpressed persistent antigen in the mouse liver and to induce liver inflammation

Title Tesim:
LIGHT induces distinct signals to clear an AAVexpressed persistent antigen in the mouse liver and to induce liver inflammation
Creator:
Washburn, Michael, Fu, Yang-Xin, Kovalev, Grigoriy I., Koroleva, Ekaterina, and Su, Lishan
Date of publication:
2010
Abstract Tesim:
Background: Infection with adeno-associated virus (AAV) vector with liver tropism leads to persistent expression of foreign antigens in the mouse liver, with no significant liver inflammation or pathology. This provides a model to investigate antigen persistence in the liver and strategies to modulate host immunity to reduce or clear the foreign antigen expressed from AAV vector in the liver. Methods/Principal Findings: We showed that expressing LIGHT with an adenovirus vector (Ad) in mice with established AAV in the liver led to clearance of the AAV. Ad-LIGHT enhanced CD8 effector T cells in the liver, correlated with liver inflammation. LTbR-Ig proteins blocked Ad-LIGHT in clearing AAV. Interestingly, in LTbR-null mice, Ad-LIGHT still cleared AAV but caused no significant liver inflammation. Conclusions/Significance: Our data suggest that LIGHT interaction with the LTbR plays a critical role in liver inflammation but is not required for LIGHT-mediated AAV clearance. These findings will shed light on developing novel immunotherapeutics in treating people chronically infected with hepato-tropic viruses.
Resource type:
Article
Affiliation Label Tesim:
Curriculum in Genetics and Molecular Biology and UNC Lineberger Comprehensive Cancer Center
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/0p38-8v47
Identifier:
https://dx.doi.org/10.1371/journal.pone.0010585
ISSN:
1932-6203
Journal Issue:
5
Journal Title:
PLoS ONE
Journal Volume:
5
Keyword:
Adeno associated virus antigen, virus antigen, herpesvirus entry mediator ligand, immunoglobulin, lymphotoxin beta receptor, protein LIGHT, and unclassified drug
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
and The University of Chicago
Person:
Washburn, Michael, Fu, Yang-Xin, Kovalev, Grigoriy I., Koroleva, Ekaterina, and Su, Lishan
Rights Statement Label:
In Copyright
Source:
gb19fc21s

1746. Infection and depletion of CD4+group-1 innate lymphoid cells by HIV-1 via type-I interferon pathway

Title Tesim:
Infection and depletion of CD4+group-1 innate lymphoid cells by HIV-1 via type-I interferon pathway
Creator:
Su, Lishan, Zhang, ligup, Fu, Qiang, Liu, Zhenwen, Li, Guangming, Zhao, Juanjuan, Zhang, Xin, Wang, Qi, Tu, Bo, Yu, Haisheng, Wang, Hongbo, Chen, Weiwei, Cheng, Liang, Sun, Yanling, and Zhang, Zheng
Date of publication:
2018
Abstract Tesim:
Innate lymphoid cells (ILCs) are severely depleted during chronic HIV-1 infection by unclear mechanisms. We report here that human ILC1s comprising of CD4+and CD4-subpopulations were present in various human lymphoid organs but with different transcription programs and functions. Importantly, CD4+ILC1s expressed HIV-1 co-receptors and were productively infected by HIV-1 in vitro and in vivo. Furthermore, chronic HIV-1 infection activated and depleted both CD4+and CD4-ILC1s, and impaired their cytokine production activity. Highly active antiretroviral (HAART) therapy in HIV-1 patients efficiently rescued the ILC1 numbers and reduced their activation, but failed to restore their functionality. We also found that blocking type-I interferon (IFN-I) signaling during HIV-1 infection in vivo in humanized mice prevented HIV-1 induced depletion or apoptosis of ILC1 cells. Therefore, we have identified the CD4+ILC1 cells as a new target population for HIV-1 infection, and revealed that IFN-I contributes to the depletion of ILC1s during HIV-1 infection.
Resource type:
Article
Affiliation Label Tesim:
UNC Lineberger Comprehensive Cancer Center
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/g8ag-0v51
Identifier:
https://dx.doi.org/10.1371/journal.ppat.1006819
ISSN:
1553-7366
Journal Issue:
1
Journal Title:
PLoS Pathogens
Journal Volume:
14
Keyword:
interleukin 18 binding protein, tumor necrosis factor, chemokine receptor CXCR4, chemokine receptor CCR5, interferon, caspase 3, and interleukin 12
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
, Chinese Academy of Science, and Beijing 302 Hospital
Person:
Su, Lishan, Zhang, ligup, Fu, Qiang, Liu, Zhenwen, Li, Guangming, Zhao, Juanjuan, Zhang, Xin, Wang, Qi, Tu, Bo, Yu, Haisheng, Wang, Hongbo, Chen, Weiwei, Cheng, Liang, Sun, Yanling, and Zhang, Zheng
Rights Statement Label:
In Copyright
Source:
9019s746p

1747. SENP3-mediated host defense response contains HBV replication and restores protein synthesis

Title Tesim:
SENP3-mediated host defense response contains HBV replication and restores protein synthesis
Creator:
Murthy, Preetish Kadur Lakshminarasimha, Han, Yan, Tung, Kuei-Ling, Shen, Xiling, Li, Xiaodong, Qian, Shu-Bing, Su, Lishan, Xi, Rui, Xin, Yongning, Liu, Botao, Wang, Zhuo, Wan, Ji, Varanko, Anastasia, Rakhilin, Nikolai, Li, Feng, and Guy, Cynthia D.
Date of publication:
2019
Abstract Tesim:
Certain organs are capable of containing the replication of various types of viruses. In the liver, infection of Hepatitis B virus (HBV), the etiological factor of Hepatitis B and hepatocellular carcinoma (HCC), often remains asymptomatic and leads to a chronic carrier state. Here we investigated how hepatocytes contain HBV replication and promote their own survival by orchestrating a translational defense mechanism via the stress-sensitive SUMO-2/3-specific peptidase SENP3. We found that SENP3 expression level decreased in HBV-infected hepatocytes in various models including HepG2-NTCP cell lines and a humanized mouse model. Downregulation of SENP3 reduced HBV replication and boosted host protein translation. We also discovered that IQGAP2, a Ras GTPase-activating-like protein, is a key substrate for SENP3-mediated de-SUMOylation. Downregulation of SENP3 in HBV infected cells facilitated IQGAP2 SUMOylation and degradation, which leads to suppression of HBV gene expression and restoration of global translation of host genes via modulation of AKT phosphorylation. Thus, The SENP3-IQGAP2 de-SUMOylation axis is a host defense mechanism of hepatocytes that restores host protein translation and suppresses HBV gene expression.
Resource type:
Article
Affiliation Label Tesim:
UNC Lineberger Comprehensive Cancer Center
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/z1er-s360
Identifier:
https://dx.doi.org/10.1371/journal.pone.0209179
ISSN:
1932-6203
Journal Issue:
1
Journal Title:
PLoS ONE
Journal Volume:
14
Keyword:
IQGAP2 protein, unclassified drug, protein kinase B, SUMO specific peptidase 3, and scaffold protein
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
Duke University, , Cornell University, Qingdao Municipal Hospital, University of Massachusetts Medical School, and Duke University School of Medicine
Person:
Murthy, Preetish Kadur Lakshminarasimha, Han, Yan, Tung, Kuei-Ling, Shen, Xiling, Li, Xiaodong, Qian, Shu-Bing, Su, Lishan, Xi, Rui, Xin, Yongning, Liu, Botao, Wang, Zhuo, Wan, Ji, Varanko, Anastasia, Rakhilin, Nikolai, Li, Feng, and Guy, Cynthia D.
Rights Statement Label:
In Copyright
Source:
3f462b85z

1748. IgG Fc-binding motif-conjugated HIV-1 fusion inhibitor exhibits improved potency and in vivo half-life: Potential application in combination with broad neutralizing antibodies

Title Tesim:
IgG Fc-binding motif-conjugated HIV-1 fusion inhibitor exhibits improved potency and in vivo half-life: Potential application in combination with broad neutralizing antibodies
Creator:
Qin, Chuan, Lu, Lu, Bi, Wenwen, Cheng, Liang, Xu, Wei, Wang, Qi, Li, Guangming, Su, Lishan, Xia, Shuai, Wang, Qian, Xue, Jing, and Jiang, Shibo
Date of publication:
2019
Abstract Tesim:
The clinical application of conventional peptide drugs, such as the HIV-1 fusion inhibitor enfuvirtide, is limited by their short half-life in vivo. To overcome this limitation, we developed a new strategy to extend the in vivo half-life of a short HIV-1 fusion inhibitory peptide, CP24, by fusing it with the human IgG Fc-binding peptide (IBP). The newly engineered peptide IBPCP24 exhibited potent and broad anti-HIV-1 activity with IC50 values ranging from 0.2 to 173.7 nM for inhibiting a broad spectrum of HIV-1 strains with different subtypes and tropisms, including those resistant to enfuvirtide. Most importantly, its half-life in the plasma of rhesus monkeys was 46.1 h, about 26- and 14-fold longer than that of CP24 (t1/2 = 1.7 h) and enfuvirtide (t1/2 = 3 h), respectively. IBP-CP24 intravenously administered in rhesus monkeys could not induce significant IBP-CP24-specific antibody response and it showed no obvious in vitro or in vivo toxicity. In the prophylactic study, humanized mice pretreated with IBPCP24 were protected from HIV-1 infection. As a therapeutic treatment, coadministration of IBP-CP24 and normal human IgG to humanized mice with chronic HIV-1 infection resulted in a significant decrease of plasma viremia. Combining IBP-CP24 with a broad neutralizing antibody (bNAb) targeting CD4-binding site (CD4bs) in gp120 or a membrane proximal external region (MPER) in gp41 exhibited synergistic effect, resulting in significant dose-reduction of the bNAb and IBP-CP24. These results suggest that IBP-CP24 has the potential to be further developed as a new HIV-1 fusion inhibitor-based, long-acting anti-HIV drug that can be used alone or in combination with a bNAb for treatment and prevention of HIV-1 infection.
Resource type:
Article
Affiliation Label Tesim:
UNC Lineberger Comprehensive Cancer Center
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/n86s-9922
Identifier:
https://dx.doi.org/10.1371/journal.ppat.1008082
ISSN:
1553-7366
Journal Issue:
12
Journal Title:
PLoS Pathogens
Journal Volume:
15
Keyword:
enfuvirtide, long acting drug, glycoprotein gp 41, n6 antibody, antivirus agent, igg fc binding peptide cp24, Fc receptor, neutralizing antibody, cp24, fc binding peptide, Human immunodeficiency virus fusion inhibitor, virus DNA, glycoprotein gp 120, and unclassified drug
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
Peking Union Medical College, Fudan University, and
Person:
Qin, Chuan, Lu, Lu, Bi, Wenwen, Cheng, Liang, Xu, Wei, Wang, Qi, Li, Guangming, Su, Lishan, Xia, Shuai, Wang, Qian, Xue, Jing, and Jiang, Shibo
Rights Statement Label:
In Copyright
Source:
ww72bh66m

1749. Interactions among poverty, gender, and health systems affect women's participation in services to prevent HIV transmission from mother to child: A causal loop analysis

Title Tesim:
Interactions among poverty, gender, and health systems affect women's participation in services to prevent HIV transmission from mother to child: A causal loop analysis
Creator:
Munthali, Alister C., Katahoire, Anne Ruhweza, Okello, Elialilia S., Thomas, James C., Lich, Kristen Hassmiller, Kadzandira, John, Flax, Valerie, and Yourkavitch, Jennifer
Date of publication:
2018
Abstract Tesim:
Retention in care remains an important issue for prevention of mother-to-child transmission (PMTCT) programs according to WHO guidelines, formerly called the ªOption B+º approach. The objective of this study was to examine how poverty, gender, and health system factors interact to influence women's participation in PMTCT services. We used qualitative research, literature, and hypothesized variable connections to diagram causes and effects in causal loop models. We found that many factors, including antiretroviral therapy (ART) use, service design and quality, stigma, disclosure, spouse/partner influence, decision- making autonomy, and knowledge about PMTCT, influence psychosocial health, which in turn affects women's participation in PMTCT services. Thus, interventions to improve psychosocial health need to address many factors to be successful. We also found that the design of PMTCT services, a modifiable factor, is important because it affects several other factors. We identified 66 feedback loops that may contribute to policy resistanceÐthat is, a policy's failure to have its intended effect. Our findings point to the need for a multipronged intervention to encourage women's continued participation in PMTCT services and for longitudinal research to quantify and test our causal loop model.
Resource type:
Article
Affiliation Label Tesim:
Carolina Population Center and Department of Health Policy and Management
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/9w5f-er49
Identifier:
https://dx.doi.org/10.1371/journal.pone.0197239
ISSN:
1932-6203
Journal Issue:
5
Journal Title:
PLoS ONE
Journal Volume:
13
Keyword:
human, nonhuman, stigma, child, poverty, quantitative analysis, gender, male, Human immunodeficiency virus, female, antiretroviral therapy, feedback system, decision making, spouse, and qualitative research
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
University of Malawi, Makerere University, and
Person:
Munthali, Alister C., Katahoire, Anne Ruhweza, Okello, Elialilia S., Thomas, James C., Lich, Kristen Hassmiller, Kadzandira, John, Flax, Valerie, and Yourkavitch, Jennifer
Rights Statement Label:
In Copyright
Source:
3t945x184

1750. HIV treatment as prevention: Debate and commentary-will early infection compromise treatment-as-prevention strategies?

Title Tesim:
HIV treatment as prevention: Debate and commentary-will early infection compromise treatment-as-prevention strategies?
Creator:
Williams, Brian G., Fraser, Christophe, Dye, Christopher, Miller, William C., Powers, Kimberly A., and Cohen, Myron S.
Date of publication:
2012
Abstract Tesim:
Universal HIV testing and immediate antiretroviral therapy for infected individuals has been proposed as a way of reducing the transmission of HIV and thereby bringing the HIV epidemic under control. It is unclear whether transmission during early HIV infection-before individuals are likely to have been diagnosed with HIV and started on antiretroviral therapy-will compromise the effectiveness of treatment as prevention. This article presents two opposing viewpoints by Powers, Miller, and Cohen, and Williams and Dye, followed by a commentary by Fraser.
Resource type:
Article
Affiliation Label Tesim:
Department of Medicine and Department of Microbiology and Immunology
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/s0wc-f607
Identifier:
https://dx.doi.org/10.1371/journal.pmed.1001232
ISSN:
1549-1277
Journal Issue:
7
Journal Title:
PLoS Medicine
Journal Volume:
9
Keyword:
anti human immunodeficiency virus agent, clinical effectiveness, epidemic, risk factor, highly active antiretroviral therapy, virus transmission, sexual transmission, virus load, Human immunodeficiency virus infection, incidence, Human immunodeficiency virus, infection risk, human, and mathematical model
Language Label:
English
License Label:
Attribution 3.0 United States
ORCID:
Other Affiliation:
South African Centre for Epidemiological Modelling and Analysis, Imperial College London, World Health Organization, and
Person:
Williams, Brian G., Fraser, Christophe, Dye, Christopher, Miller, William C., Powers, Kimberly A., and Cohen, Myron S.
Rights Statement Label:
In Copyright
Source:
w6634863z