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Kathryn Anastos

Bio: Kathryn Anastos is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Acquired immunodeficiency syndrome (AIDS) & Women's Interagency HIV Study. The author has an hindex of 59, co-authored 351 publications receiving 13391 citations. Previous affiliations of Kathryn Anastos include Lincoln Hospital & Capital Medical University.


Papers
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Journal ArticleDOI
10 Dec 2010-Science
TL;DR: Differences in binding to viral peptide antigens by HLA may be the major factors underlying genetic differences between HIV controllers and progressors, and genome-wide association results implicate the nature of the HLA–viral peptide interaction as the major factor modulating durable control of HIV infection.
Abstract: Infectious and inflammatory diseases have repeatedly shown strong genetic associations within the major histocompatibility complex (MHC); however, the basis for these associations remains elusive. To define host genetic effects on the outcome of a chronic viral infection, we performed genome-wide association analysis in a multiethnic cohort of HIV-1 controllers and progressors, and we analyzed the effects of individual amino acids within the classical human leukocyte antigen (HLA) proteins. We identified >300 genome-wide significant single-nucleotide polymorphisms (SNPs) within the MHC and none elsewhere. Specific amino acids in the HLA-B peptide binding groove, as well as an independent HLA-C effect, explain the SNP associations and reconcile both protective and risk HLA alleles. These results implicate the nature of the HLA-viral peptide interaction as the major factor modulating durable control of HIV infection.

1,038 citations

Journal ArticleDOI
TL;DR: In HIV-positive women, plasma HIV RNA level and CD4+ count in combination appear to have a strong and statistically interactive association with incident detection of HPV, some of which may reflect HPV reactivation (e.g., in sexually inactive women).
Abstract: Background: Little is known in human immunodeficiency virus (HIV)-positive women about how the combination of plasma HIV RNA level and CD4 + T-cell count is associated with the natural history of human papillomavirus (HPV) infection or about HPV reactivation-whether it occurs and with what frequency in HIV-positive women. Methods: HIV-positive (n = 1848) and -negative (n = 514) women were assessed at semiannual visits (total person-years = 5661) for cervicovaginal HPV with polymerase chain reaction assays and for squamous intraepithelial lesions (SILs) by Pap smear. We studied the prevalent detection of HPV and SILs with generalized estimating equations and the incident detection and persistence of HPV and SILs with multivariable Cox models. All statistical tests were two-sided. Results: We observed a strong interaction between the associations of CD4 + and plasma HIV RNA strata with both prevalent (P interaction = .002) and incident (P interaction = .001) detection of HPV. Indeed, the hazard ratio for incident HPV detection peaked between 4.0 and 5.0, with either a CD4 + count of less than 200 cells per mm 3 or an HIV RNA level of more than 100000 copies per mL. Although incident HPV detection in all women was associated with the number of recent sex partners (P trend <.001), 22% of sexually inactive HIV-positive women with a CD4 + count of less than 200 cells/mm 3 also had at least one incidently detected HPV type. The association between CD4 + /HIV RNA strata and HPV persistence was statistically significantly smaller (P<.001) than for incident HPV detection. SIL prevalence, incident detection, and persistence had similar associations with CD4 + /HIV RNA strata as HPV (above). Conclusion: In HIV-positive women, plasma HIV RNA level and CD4 + count in combination appear to have a strong and statistically interactive association with incident detection of HPV, some of which may reflect HPV reactivation (e.g., in sexually inactive women). The more moderate association between HIV coinfection and HPV persistence could partly explain why cervical cancer rates have not reached more epidemic proportions in HIV-positive women.

511 citations

Journal ArticleDOI
TL;DR: The data support the hypothesis of a continuum of risk, with early childhood abuse leading to later domestic violence, which may increase the risk of behaviors leading to HIV infection.
Abstract: OBJECTIVES: The purpose of this study was to determine the prevalence and effect of domestic violence and childhood sexual abuse in women with HIV or at risk for HIV infection. METHODS: Participants with HIV or at risk for HIV infection enrolled in the Women's Interagency HIV Study. Childhood sexual abuse; all physical, sexual, and coercive violence by a partner; HIV serostatus; demographic data; and substance use and sexual habits were assessed. RESULTS: The lifetime prevalence of domestic violence was 66% and 67%, respectively, in 1288 women with HIV and 357 uninfected women. One quarter of the women reported recent abuse, and 31% of the HIV-seropositive women and 27% of the HIV-seronegative women reported childhood sexual abuse. Childhood sexual abuse was strongly associated with a lifetime history of domestic violence and high-risk behaviors, including using drugs, having more than 10 male sexual partners and having male partners at risk for HIV infection, and exchanging sex for drugs, money, or shelter. CONCLUSIONS: Our data support the hypothesis of a continuum of risk, with early childhood abuse leading to later domestic violence, which may increase the risk of behaviors leading to HIV infection. Language: en

361 citations

Journal ArticleDOI
TL;DR: To estimate the net effect of highly active antiretroviral therapy (HAART) on time to acquired immunodeficiency syndrome (AIDS) or death, the authors used inverse probability-of-treatment weighted estimation of a marginal structural model, which can appropriately adjust for time-varying confounders affected by prior treatment or exposure.
Abstract: To estimate the net (i.e., overall) effect of highly active antiretroviral therapy (HAART) on time to acquired immunodeficiency syndrome (AIDS) or death, the authors used inverse probability-of-treatment weighted estimation of a marginal structural model, which can appropriately adjust for time-varying confounders affected by prior treatment or exposure. Human immunodeficiency virus (HIV)-positive men and women (n = 1,498) were followed in two ongoing cohort studies between 1995 and 2002. Sixty-one percent (n = 918) of the participants initiated HAART during 6,763 person-years of follow-up, and 382 developed AIDS or died. Strong confounding by indication for HAART was apparent; the unadjusted hazard ratio for AIDS or death was 0.98. The hazard ratio from a standard time-dependent Cox model that included time-varying CD4 cell count, HIV RNA level, and other time-varying and fixed covariates as regressors was 0.81 (95% confidence interval: 0.61, 1.07). In contrast, the hazard ratio from a marginal structural survival model was 0.54 (robust 95% confidence interval: 0.38, 0.78), suggesting a clinically meaningful net benefit of HAART. Standard Cox analysis failed to detect a clear net benefit, because it does not appropriately adjust for time-dependent covariates, such as HIV RNA level and CD4 cell count, that are simultaneously confounders and intermediate variables.

276 citations

Journal ArticleDOI
20 Aug 2008-AIDS
TL;DR: Beyond traditional cardiovascular disease risk factors, low CD4+ T-cell count is the most robust risk factor for increased subclinical carotid atherosclerosis in HIV-infected women and men.
Abstract: Recent studies among HIV-infected populations have linked use of combination antiretroviral therapy with increased risk of cardiovascular disease (CVD) events [1-4] and subclinical atherosclerosis [5-7]. Among HIV-infected individuals, low CD4+ T-cell count has also been identified as a vascular risk factor [5]. However, the data have not been consistent as other studies have not confirmed the reported associations of antiretroviral use [8-11] or low CD4+ T-cell count [2] with clinical or subclinical CVD. Several potential mechanisms have been described that may link HIV disease and its treatment with increased risk of vascular disease. Individuals with untreated HIV infection have decreased levels of high-density lipoprotein cholesterol (HDL-C) and increased levels of triglycerides [12-14], which are adverse risk factors for vascular disease. On the other hand, persons with untreated HIV infection also have reductions in low-density lipoprotein cholesterol (LDL-C) and total cholesterol, which may be favorable characteristics with regard to atherosclerotic risk [12-14]. Initiation of antiretroviral therapy tends to normalize lipid parameters (total cholesterol, LDL-C and triglycerides, but not HDL-C) [14]. Some therapies, notably protease inhibitors (PI), may have adverse effects on LDL-C and triglyceride levels, blood pressure, and risk of diabetes [15-19]. Use of nucleoside analogs has been associated with body fat changes, insulin resistance and diabetes [20-22]. Circulating markers of inflammation such as C-reactive protein (CRP) may be elevated among individuals with HIV infection, especially during progression to AIDS [23]. The purpose of the present investigation was to assess the association of HIV infection, HIV disease parameters (including CD4+ T-cell counts, HIV viral load, and AIDS) and antiretroviral medication use with subclinical vascular disease. We report the results from two studies, conducted in parallel, within the Women's Interagency HIV Study (WIHS) and the Multicenter AIDS Cohort Study (MACS). WIHS and MACS are population-based US cohort studies that offer several important strengths, including large sample size, inclusion of HIV-uninfected persons who were recruited from the same at-risk populations as the HIV-infected individuals, and extensive longitudinal, protocol-driven data collection on clinical, behavioral, and demographic variables. The present report describes data from the baseline phase of a WIHS-MACS Carotid Ultrasound Substudy, which features standardized image acquisition and measurement of carotid artery intima-media thickness, a quantitative measure of atherosclerosis burden.

251 citations


Cited by
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Journal ArticleDOI
TL;DR: The 11th edition of Harrison's Principles of Internal Medicine welcomes Anthony Fauci to its editorial staff, in addition to more than 85 new contributors.
Abstract: The 11th edition of Harrison's Principles of Internal Medicine welcomes Anthony Fauci to its editorial staff, in addition to more than 85 new contributors. While the organization of the book is similar to previous editions, major emphasis has been placed on disorders that affect multiple organ systems. Important advances in genetics, immunology, and oncology are emphasized. Many chapters of the book have been rewritten and describe major advances in internal medicine. Subjects that received only a paragraph or two of attention in previous editions are now covered in entire chapters. Among the chapters that have been extensively revised are the chapters on infections in the compromised host, on skin rashes in infections, on many of the viral infections, including cytomegalovirus and Epstein-Barr virus, on sexually transmitted diseases, on diabetes mellitus, on disorders of bone and mineral metabolism, and on lymphadenopathy and splenomegaly. The major revisions in these chapters and many

6,968 citations

Journal ArticleDOI
24 Mar 2010-BMJ
TL;DR: This update of the CONSORT statement improves the wording and clarity of the previous checklist and incorporates recommendations related to topics that have only recently received recognition, such as selective outcome reporting bias.
Abstract: Overwhelming evidence shows the quality of reporting of randomised controlled trials (RCTs) is not optimal. Without transparent reporting, readers cannot judge the reliability and validity of trial findings nor extract information for systematic reviews. Recent methodological analyses indicate that inadequate reporting and design are associated with biased estimates of treatment effects. Such systematic error is seriously damaging to RCTs, which are considered the gold standard for evaluating interventions because of their ability to minimise or avoid bias. A group of scientists and editors developed the CONSORT (Consolidated Standards of Reporting Trials) statement to improve the quality of reporting of RCTs. It was first published in 1996 and updated in 2001. The statement consists of a checklist and flow diagram that authors can use for reporting an RCT. Many leading medical journals and major international editorial groups have endorsed the CONSORT statement. The statement facilitates critical appraisal and interpretation of RCTs. During the 2001 CONSORT revision, it became clear that explanation and elaboration of the principles underlying the CONSORT statement would help investigators and others to write or appraise trial reports. A CONSORT explanation and elaboration article was published in 2001 alongside the 2001 version of the CONSORT statement. After an expert meeting in January 2007, the CONSORT statement has been further revised and is published as the CONSORT 2010 Statement. This update improves the wording and clarity of the previous checklist and incorporates recommendations related to topics that have only recently received recognition, such as selective outcome reporting bias. This explanatory and elaboration document-intended to enhance the use, understanding, and dissemination of the CONSORT statement-has also been extensively revised. It presents the meaning and rationale for each new and updated checklist item providing examples of good reporting and, where possible, references to relevant empirical studies. Several examples of flow diagrams are included. The CONSORT 2010 Statement, this revised explanatory and elaboration document, and the associated website (www.consort-statement.org) should be helpful resources to improve reporting of randomised trials.

5,957 citations

Journal ArticleDOI
09 Jan 2013-BMJ
TL;DR: The SPIRIT 2013 Explanation and Elaboration paper provides important information to promote full understanding of the checklist recommendations and strongly recommends that this explanatory paper be used in conjunction with the SPIRit Statement.
Abstract: High quality protocols facilitate proper conduct, reporting, and external review of clinical trials. However, the completeness of trial protocols is often inadequate. To help improve the content and quality of protocols, an international group of stakeholders developed the SPIRIT 2013 Statement (Standard Protocol Items: Recommendations for Interventional Trials). The SPIRIT Statement provides guidance in the form of a checklist of recommended items to include in a clinical trial protocol. This SPIRIT 2013 Explanation and Elaboration paper provides important information to promote full understanding of the checklist recommendations. For each checklist item, we provide a rationale and detailed description; a model example from an actual protocol; and relevant references supporting its importance. We strongly recommend that this explanatory paper be used in conjunction with the SPIRIT Statement. A website of resources is also available (www.spirit-statement.org). The SPIRIT 2013 Explanation and Elaboration paper, together with the Statement, should help with the drafting of trial protocols. Complete documentation of key trial elements can facilitate transparency and protocol review for the benefit of all stakeholders.

3,108 citations

Journal ArticleDOI
TL;DR: For example, this article found that exposure to multiple types and repeated episodes of maltreatment is associated with increased risks of severe maltreatment and psychological consequences, which has longlasting effects on mental health, drug and alcohol misuse (especially in girls), risky sexual behaviour, obesity, and criminal behaviour.

3,034 citations

Journal ArticleDOI
TL;DR: Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection, and the degree of association increased with the number of vaginal-sex and oral-sex partners, among subjects with or without the established risk factors of tobacco and alcohol use.
Abstract: BACKGROUND Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic data have been inconsistent. METHODS We performed a hospital-based, case-control study of 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer to evaluate associations between HPV infection and oropharyngeal cancer. Multivariate logistic-regression models were used for case-control comparisons. RESULTS A high lifetime number of vaginal-sex partners (26 or more) was associated with oropharyngeal cancer (odds ratio, 3.1; 95% confidence interval [CI], 1.5 to 6.5), as was a high lifetime number of oral-sex partners (6 or more) (odds ratio, 3.4; 95% CI, 1.3 to 8.8). The degree of association increased with the number of vaginal-sex and oral-sex partners (P values for trend, 0.002 and 0.009, respectively). Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection (odds ratio, 14.6; 95% CI, 6.3 to 36.6), oral infection with any of 37 types of HPV (odds ratio, 12.3; 95% CI, 5.4 to 26.4), and seropositivity for the HPV-16 L1 capsid protein (odds ratio, 32.2; 95% CI, 14.6 to 71.3). HPV-16 DNA was detected in 72% (95% CI, 62 to 81) of 100 paraffin-embedded tumor specimens, and 64% of patients with cancer were seropositive for the HPV-16 oncoprotein E6, E7, or both. HPV-16 L1 seropositivity was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use (odds ratio, 19.4; 95% CI, 3.3 to 113.9) and among those without such a history (odds ratio, 33.6; 95% CI, 13.3 to 84.8). The association was similarly increased among subjects with oral HPV-16 infection, regardless of their tobacco and alcohol use. By contrast, tobacco and alcohol use increased the association with oropharyngeal cancer primarily among subjects without exposure to HPV-16. CONCLUSIONS Oral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use.

2,529 citations