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David E. Soper - One of the best experts on this subject based on the ideXlab platform.
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Association of Lower Genital Tract Inflammation With Objective Evidence of Endometritis
2013Co-Authors: Jeffrey F. Peipert, Roberta B Ness, David E. Soper, Debra BassAbstract:The purpose of this report is to evaluate the association between lower Genital Tract Inflammation and objectively diagnosed endometritis. We analyzed the first 157 patients enrolled in the PEACH study, a multicenter randomized clinical trial designed to compare the effectiveness of outpatient and inpatient therapy for PID. Women less than 38 years of age, who presented with a history of pelvic discomfort for 30 days or less and who were found to have pelvic organ tenderness (uterine or adnexal tenderness) on bimanual examination, were initially invited to participate. After recruitment of the first 58 patients (group 1) we added the presence of leukorrhea, mucopurulent cervicitis, or untreated positive test for N. gonorrhoeae or C. trachomatis to the inclusion criteria (group 2, N 99). We compared rates of endometritis in the two groups and calculated the sensitivity, specificity, and predicted values of the presence of white blood cells in the vaginal wet preparation. The rate of upper Genital Tract infection in group 1 was 46.5 % (27/58) compared to 49.5 % (49/99) in group 2. Microbiologic evidence of either N. gonorrhoeae or C. trachomatis increased from 22.4 % in group 1 to 38.3 % in group 2. The presence of Vaginal white blood cells or mueopus has a high sensitivity (88.9%), but a low specificity (19.4%) for the diagnosis of upper Genital-Tract infection. Assessment of the lower Genital Tract for evidence of infection or Inflammation is a valuable component of the diagnostic evaluation of pelvic inflammatory disease. The presence of either mucopus or vaginal white blood cells is a highly sensitive test for endometritis in patients with pelvic pain and tenderness
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pelvic inflammatory disease
Obstetrics & Gynecology, 2010Co-Authors: David E. SoperAbstract:Pelvic inflammatory disease (PID) is an infection-caused inflammatory continuum from the cervix to the peritoneal cavity. Most importantly, it is associated with fallopian tube Inflammation, which can lead to infertility, ectopic pregnancy, and chronic pelvic pain. The microbial etiology is linked to sexually transmitted microorganisms, including Chlamydia trachomatis, Neisseria gonorrheae, Mycoplasma Genitalium, and bacterial vaginosis-associated microorganisms, predominantly anaerobes. Pelvic pain and fever are commonly absent in women with confirmed PID. Clinicians should consider milder symptoms such as abnormal vaginal discharge, metrorrhagia, postcoital bleeding, and urinary frequency as potential symptoms associated with the disease, particularly in women at risk of sexually transmitted infection. The diagnosis of PID is based on the findings of lower Genital Tract Inflammation associated with pelvic organ tenderness. The outpatient treatment of mild-to-moderate PID should include tolerated antibiotic regimens with activity against the commonly isolated microorganisms associated with PID and usually consists of an extended spectrum cephalosporin in conjunction with either doxycycline or azithromycin. Clinically severe PID should prompt hospitalization and imaging to rule out a tuboovarian abscess. Parenteral broad-spectrum antibiotic therapy with activity against a polymicrobial flora, particularly gram-negative aerobes and anaerobes, should be implemented. Screening for and treatment of Chlamydia infection can prevent PID.
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Association of Lower Genital Tract Inflammation With Objective Evidence of Endometritis
Hindawi Limited, 2000Co-Authors: Jeffrey F. Peipert, Roberta B Ness, David E. Soper, Debra BassAbstract:The purpose of this report is to evaluate the association between lower Genital Tract Inflammation and objectively diagnosed endometritis. We analyzed the first 157 patients enrolled in the PEACH study, a multicenter randomized clinical trial designed to compare the effectiveness of outpatient and inpatient therapy for PID. Women less than 38 years of age, who presented with a history of pelvic discomfort for 30 days or less and who were found to have pelvic organ tenderness (uterine or adnexal tenderness) on bimanual examination, were initially invited to participate. After recruitment of the first 58 patients (group 1) we added the presence of leukorrhea, mucopurulent cervicitis, or untreated positive test for N. gonorrhoeae or C. trachomatis to the inclusion criteria (group 2, N = 99). We compared rates of endometritis in the two groups and calculated the sensitivity, specificity, and predicted values of the presence of white blood cells in the vaginal wet preparation. The rate of upper Genital Tract infection in group 1 was 46.5% (27/58) compared to 49.5% (49/99) in group 2. Microbiologic evidence of either N. gonorrhoeae or C. trachomatis increased from 22.4% in group 1 to 38.3% in group 2. The presence of Vaginal white blood cells or mueopus has a high sensitivity (88.9%), but a low specificity (19.4%) for the diagnosis of upper Genital-Tract infection. Assessment of the lower Genital Tract for evidence of infection or Inflammation is a valuable component of the diagnostic evaluation of pelvic inflammatory disease. The presence of either mucopus or vaginal white blood cells is a highly sensitive test for endometritis in patients with pelvic pain and tenderness. Infect. Dis. Obstet. Gynecol. 8:83–87, 2000
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Factors Predicting Upper Genital Tract Inflammation among Women with Lower Genital Tract Infection
Journal of women's health, 1998Co-Authors: Deborah B. Nelson, Roberta B Ness, Jeffrey F. Peipert, David E. Soper, Julie Gluck, Harold C. Wiesenfeld, Peter A. RiceAbstract:This study identified factors that discriminate between women with a lower Genital Tract infection (LGTI) and women with a LGTI and endometritis. Study samples included 214 women of which 84.6% were African American with a mean age of 24.2 years who were at risk for LGTI with Chlamydia trachomatis or Neisseria gonorrhea. The primary comparison was between women having a lower Genital Tract infection without endometritis and women having a lower Genital Tract infection with endometritis. Women with LGTI and endometritis were older and reported a history of more sexually transmitted diseases abdominal pain and use of barrier methods of contraception than women with LGTI alone. The regression model found that women with LGTI and endometritis were 7.1 times more likely to report abdominal pain and 4.6 times more likely to use barrier methods of contraception than women with LGTI alone. The results indicate that behavioral factors in addition to symptoms can be used to identify women with and without upper Genital Tract involvement.
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pelvic inflammatory disease
Infectious Disease Clinics of North America, 1994Co-Authors: David E. SoperAbstract:The pathophysiology of pelvic inflammatory disease (PID) involves an ascending infection of cervicovaginal microorganisms, of which the most important pathogens are Neisseria gonorrhoeae and Chlamydia trachomatis. The clinician should recognize that not all women with PID will present with abdominal pain and that associated atypical symptoms such as meteorrhagia and dyspareunia should suggest diagnosis. The documentation of lower Genital Tract Inflammation is helpful in making the diagnosis of PID. Treatment with broad spectrum antibiotic regimens is currently recommended. Prevention of sexually transmitted diseases and ascending infection remains of utmost importance to decrease the sequelae, such as tubal factor infertility and ectopic pregnancy associated with PID.
Jo Ann S. Passmore - One of the best experts on this subject based on the ideXlab platform.
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pl05 2 why sti associated Genital Tract Inflammation still matters in hiv transmission
Sexually Transmitted Infections, 2015Co-Authors: Jo Ann S. PassmoreAbstract:Women in Africa, especially young women, have very high HIV incidence rates that cannot be fully explained by behavioural risks. In the setting of syndromic management for sexually transmitted infections (STIs) and bacterial vaginosis (BV), the influence of these, particularly asymptomatic infections, on CD4+ T cell activation and Inflammation in the Genital Tracts of adolescents from South Africa urgently needs to be addressed. The influence of Genital Inflammation on HIV acquisition in this group will be discussed. Our study found that HIV seroconversion was associated with raised Genital inflammatory cytokines (including chemokines MIP-1α, MIP-1β and IP-10). The risk of HIV acquisition was significantly higher in women with evidence of Genital Inflammation, defined by at least 5 of 9 inflammatory cytokines being raised [OR 3.2; 95% confidence interval 1.3–7.9]. Genital cytokine concentrations were persistently raised (for about one year before infection), with no readily identifiable cause despite extensive investigation of several potential factors, including STIs and systemic cytokines. Adolescents (median 18 years) had significantly higher frequencies of activated CD4+ T-cells (CD38+, HLADR+, CD38+HLADR+) from cervical cytobrushes than adults, although CCR5 expression was higher in adults. STIs and BV prevalence was very high in certain areas of South Africa, with 71% of adolescents having >1 STI and/or BV, and 42% being C. trachomatis positive. Adolescents with an STI had higher frequencies of activated and proliferating T-cells compared to those with no STI/BV. Higher cervical T-cell activation marker expression was directly associated with increased Genital cytokine profiles. Our data suggests that elevated Genital concentrations of HIV target cell-recruiting chemokines and a Genital inflammatory profile contributes to the high risk of HIV acquisition in these African women. In adolescents, heightened levels of Genital immune activation and Inflammation, partly due to the presence of asymptomatic STIs/BV, could increase their risk for HIV infection.
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the role of dendritic cells in driving Genital Tract Inflammation and hiv transmission risk are there opportunities to intervene
Innate Immunity, 2015Co-Authors: Muki Shey, Nigel Garrett, Lyle R Mckinnon, Jo Ann S. PassmoreAbstract:Effective prevention of new HIV infections will require understanding the mechanisms involved in HIV acquisition. HIV transmission across the female Genital Tract is the major mode of new HIV infections in Sub-Saharan Africa and involves complex processes including cell activation, Inflammation, and recruitment of HIV target cells. Activated CD4+ T cells, dendritic cells, and macrophages have been described as targets for HIV at the Genital mucosa. Activation of these cells may occur in the presence of sexually-transmitted infections, disturbances of commensal flora, and other inflammatory processes. In this review, we discuss causes and consequences of Inflammation in the female Genital Tract, with a focus on dendritic cells. We describe the central role these cells may play in facilitating or preventing HIV transmission across the Genital mucosa, and in the initial recognition of HIV and other pathogens, allowing activation of an adaptive immune response to infection. We discuss studies that investigate interventions to limit dendritic cell activation, Inflammation and HIV transmission. This knowledge is essential in the development of novel strategies for effective HIV control including microbicides and pre-exposure prophylaxis.
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Genital Tract Inflammation during early hiv 1 infection predicts higher plasma viral load set point in women
The Journal of Infectious Diseases, 2012Co-Authors: Lindi Roberts, Carolyn Williamson, Jo Ann S. Passmore, Koleka Mlisana, Francesca Little, Lisa M Bebell, Gerhard Walzl, Melissarose AbrahamsAbstract:In sub-Saharan Africa, which has the highest prevalence of human immunodeficiency virus type 1 (HIV-1) worldwide, most new infections occur by sexual transmission to women [1]. The Genital mucosa is the initial site of viral replication following vaginal transmission of HIV-1 in women and simian immunodeficiency virus (SIV) in rhesus macaques [2, 3]. In macaques, vaginal inoculation with SIV is followed by proinflammatory cytokine production and recruitment of CD4+ T cells that are necessary for local viral expansion and dissemination to the systemic compartment [4–6]. Proinflammatory cytokine expression in the Genital mucosa correlates with viral replication and approaches baseline as peak SIV viremia declines [6]. HIV-1 infection may likewise be accompanied by an early inflammatory cascade in the Genital Tract that is associated with viral replication in this compartment. HIV-1 has been shown to directly induce inflammatory cytokine production via Toll-like receptor 7 and 8 activation [7]. Elevated concentrations of inflammatory cytokines in turn may upregulate HIV-1 replication by recruiting and activating target cells and through NF-κB activation [4, 8–11]. Several studies have shown that cervicovaginal proinflammatory cytokines are upregulated in women with early or chronic HIV-1 infection compared with HIV-uninfected women [10, 12–16]. However this upregulation may be attributed to the high frequency of sexually transmitted infections (STIs) or bacterial vaginosis (BV) in these individuals rather than HIV-1 itself [17]. For example, BV was associated with increased concentrations of proinflammatory interleukin (IL)–1β, whereas chronic HIV-1 infection was not [18]. HIV-1 shedding, which is associated with STIs [19], may induce further inflammatory cytokine production. Plasma cytokine concentrations during early HIV-1 infection are predictive of plasma viral load set points and CD4 depletion [20], and treatment with cytokines such as IL-12p70 and IL-15 during acute SIV infection is associated with altered disease course in macaques [21–23]. Several studies have suggested that cytokine responses in the Genital Tract during the early stages of HIV-1 infection may likewise be associated with disease progression. In macaques, induction of inflammatory cytokines and immune cell influx into the Genital Tract prior to vaginal SIV inoculation was associated with increased plasma viral load set points [24]. This suggests that preexisting Genital Inflammation in humans may similarly influence HIV-1 disease progression. Zara et al [14] demonstrated that upregulation of IL-1β in the Genital Tracts of HIV-1–infected women was associated with increased plasma viral loads. Recently, we reported that elevated proinflammatory cytokines in cervicovaginal lavage (CVL) correlated with lower blood CD4+ T-cell counts during early HIV-1 infection [15]. In this study, the relationships between Genital cytokine concentrations during early HIV-1 infection and plasma viral load set point and blood CD4+ T-cell counts 12 months postinfection were investigated.
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Symptomatic vaginal discharge is a poor predictor of sexually transmitted infections and Genital Tract Inflammation in high-risk women in South Africa
Journal of Infectious Diseases, 2012Co-Authors: Koleka Mlisana, Nivashnee Naicker, Lise Werner, Lindi Roberts, Francois Van Loggerenberg, A. Willem Sturm, Anneke C. Grobler, Cheryl Baxter, Jo Ann S. Passmore, Carolyn WilliamsonAbstract:BACKGROUND: Diagnosis and treatment of sexually transmitted infections (STIs) is a public health priority, particularly in regions where the incidence of human immunodeficiency virus (HIV) infection is high. In most developing countries, STIs are managed syndromically. We assessed the adequacy of syndromic diagnosis of STIs, compared with laboratory diagnosis of STIs, and evaluated the association between STI diagnosis and the risk of HIV acquisition in a cohort of high-risk women.\n\nMETHODS: HIV-uninfected high-risk women (n = 242) were followed for 24 months. Symptoms of STIs were recorded, and laboratory diagnosis of common STI pathogens was conducted every 6 months. Forty-two cytokines were measured by Luminex in cervicovaginal lavage specimens at enrollment. Human immunodeficiency virus type 1 (HIV-1) infection was evaluated monthly.\n\nRESULTS: Only 12.3% of women (25 of 204) who had a laboratory-diagnosed, discharge-causing STI had clinically evident discharge. Vaginal discharge was thus a poor predictor of laboratory-diagnosed STIs (sensitivity, 12.3%; specificity, 93.8%). Cervicovaginal cytokine concentrations did not differ between women with asymptomatic STIs and those with symptomatic STIs and were elevated in women with asymptomatic STIs, compared with women with no STIs or bacterial vaginosis. Although laboratory-diagnosed STIs were associated with increased risk of HIV infection (hazard ratio, 3.3 [95% confidence interval, 1.5-7.2)], clinical symptoms were not.\n\nCONCLUSIONS: Syndromic STI diagnosis dependent on vaginal discharge was poorly predictive of laboratory-diagnosed STI. Laboratory-diagnosed STIs were associated with increased susceptibility to HIV acquisition, while vaginal discharge was not.
Koleka Mlisana - One of the best experts on this subject based on the ideXlab platform.
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defining Genital Tract cytokine signatures of sexually transmitted infections and bacterial vaginosis in women at high risk of hiv infection a cross sectional study
Sexually Transmitted Infections, 2014Co-Authors: Lise Werner, Koleka Mlisana, Nonhlanhla N Mkhize, Lindi Masson, Francesca Little, Katharina RonacherAbstract:Objectives Sexually transmitted infections (STI) and bacterial vaginosis (BV) cause female Genital Tract Inflammation. This Inflammation, which is often present in the absence of symptoms, is associated with increased susceptibility to HIV infection. We aimed to evaluate Genital cytokine profiles and the degree of Inflammation associated with common STIs and BV. Methods HIV-uninfected women (n=227) were screened for BV, Chlamydia trachomatis , Neisseria gonorrhoeae , Herpes simplex virus type 2 (HSV-2), and Trichomonas vaginalis . Concentrations of 42 cytokines in cervicovaginal lavages and 13 cytokines in plasma were measured using Luminex. Changes in cytokine profiles were evaluated using Mann–Whitney U test, logistic regression and factor analysis. p Values were adjusted for multiple comparisons using a false discovery rate step-down procedure. Results Women with chlamydia or gonorrhoea had the highest Genital cytokine concentrations, with 17/42 and 14/42 cytokines upregulated compared with women with no infection, respectively. BV was associated with elevated proinflammatory cytokine concentrations, but lower chemokine and haematopoietic cytokine concentrations. HSV-2 reactivation was associated with lower levels of Inflammation, while trichomoniasis did not cause significant differences in Genital cytokine concentrations. Genital infections did not influence plasma cytokine concentrations. Although certain STIs, in particular chlamydia and gonorrhoea, were associated with high Genital cytokine concentrations, only 19% of women with an STI/BV had clinical signs. Conclusions Chlamydia was associated with the highest Genital cytokine levels, followed by gonorrhoea, HSV-2, trichomoniasis, and BV. In regions where HIV is prevalent and STIs are managed syndromically, better STI/BV screening is urgently needed, as certain infections were found to be highly inflammatory.
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Genital Tract Inflammation during early hiv 1 infection predicts higher plasma viral load set point in women
The Journal of Infectious Diseases, 2012Co-Authors: Lindi Roberts, Carolyn Williamson, Jo Ann S. Passmore, Koleka Mlisana, Francesca Little, Lisa M Bebell, Gerhard Walzl, Melissarose AbrahamsAbstract:In sub-Saharan Africa, which has the highest prevalence of human immunodeficiency virus type 1 (HIV-1) worldwide, most new infections occur by sexual transmission to women [1]. The Genital mucosa is the initial site of viral replication following vaginal transmission of HIV-1 in women and simian immunodeficiency virus (SIV) in rhesus macaques [2, 3]. In macaques, vaginal inoculation with SIV is followed by proinflammatory cytokine production and recruitment of CD4+ T cells that are necessary for local viral expansion and dissemination to the systemic compartment [4–6]. Proinflammatory cytokine expression in the Genital mucosa correlates with viral replication and approaches baseline as peak SIV viremia declines [6]. HIV-1 infection may likewise be accompanied by an early inflammatory cascade in the Genital Tract that is associated with viral replication in this compartment. HIV-1 has been shown to directly induce inflammatory cytokine production via Toll-like receptor 7 and 8 activation [7]. Elevated concentrations of inflammatory cytokines in turn may upregulate HIV-1 replication by recruiting and activating target cells and through NF-κB activation [4, 8–11]. Several studies have shown that cervicovaginal proinflammatory cytokines are upregulated in women with early or chronic HIV-1 infection compared with HIV-uninfected women [10, 12–16]. However this upregulation may be attributed to the high frequency of sexually transmitted infections (STIs) or bacterial vaginosis (BV) in these individuals rather than HIV-1 itself [17]. For example, BV was associated with increased concentrations of proinflammatory interleukin (IL)–1β, whereas chronic HIV-1 infection was not [18]. HIV-1 shedding, which is associated with STIs [19], may induce further inflammatory cytokine production. Plasma cytokine concentrations during early HIV-1 infection are predictive of plasma viral load set points and CD4 depletion [20], and treatment with cytokines such as IL-12p70 and IL-15 during acute SIV infection is associated with altered disease course in macaques [21–23]. Several studies have suggested that cytokine responses in the Genital Tract during the early stages of HIV-1 infection may likewise be associated with disease progression. In macaques, induction of inflammatory cytokines and immune cell influx into the Genital Tract prior to vaginal SIV inoculation was associated with increased plasma viral load set points [24]. This suggests that preexisting Genital Inflammation in humans may similarly influence HIV-1 disease progression. Zara et al [14] demonstrated that upregulation of IL-1β in the Genital Tracts of HIV-1–infected women was associated with increased plasma viral loads. Recently, we reported that elevated proinflammatory cytokines in cervicovaginal lavage (CVL) correlated with lower blood CD4+ T-cell counts during early HIV-1 infection [15]. In this study, the relationships between Genital cytokine concentrations during early HIV-1 infection and plasma viral load set point and blood CD4+ T-cell counts 12 months postinfection were investigated.
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Symptomatic vaginal discharge is a poor predictor of sexually transmitted infections and Genital Tract Inflammation in high-risk women in South Africa
Journal of Infectious Diseases, 2012Co-Authors: Koleka Mlisana, Nivashnee Naicker, Lise Werner, Lindi Roberts, Francois Van Loggerenberg, A. Willem Sturm, Anneke C. Grobler, Cheryl Baxter, Jo Ann S. Passmore, Carolyn WilliamsonAbstract:BACKGROUND: Diagnosis and treatment of sexually transmitted infections (STIs) is a public health priority, particularly in regions where the incidence of human immunodeficiency virus (HIV) infection is high. In most developing countries, STIs are managed syndromically. We assessed the adequacy of syndromic diagnosis of STIs, compared with laboratory diagnosis of STIs, and evaluated the association between STI diagnosis and the risk of HIV acquisition in a cohort of high-risk women.\n\nMETHODS: HIV-uninfected high-risk women (n = 242) were followed for 24 months. Symptoms of STIs were recorded, and laboratory diagnosis of common STI pathogens was conducted every 6 months. Forty-two cytokines were measured by Luminex in cervicovaginal lavage specimens at enrollment. Human immunodeficiency virus type 1 (HIV-1) infection was evaluated monthly.\n\nRESULTS: Only 12.3% of women (25 of 204) who had a laboratory-diagnosed, discharge-causing STI had clinically evident discharge. Vaginal discharge was thus a poor predictor of laboratory-diagnosed STIs (sensitivity, 12.3%; specificity, 93.8%). Cervicovaginal cytokine concentrations did not differ between women with asymptomatic STIs and those with symptomatic STIs and were elevated in women with asymptomatic STIs, compared with women with no STIs or bacterial vaginosis. Although laboratory-diagnosed STIs were associated with increased risk of HIV infection (hazard ratio, 3.3 [95% confidence interval, 1.5-7.2)], clinical symptoms were not.\n\nCONCLUSIONS: Syndromic STI diagnosis dependent on vaginal discharge was poorly predictive of laboratory-diagnosed STI. Laboratory-diagnosed STIs were associated with increased susceptibility to HIV acquisition, while vaginal discharge was not.
Carolyn Williamson - One of the best experts on this subject based on the ideXlab platform.
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Genital Tract Inflammation during early hiv 1 infection predicts higher plasma viral load set point in women
The Journal of Infectious Diseases, 2012Co-Authors: Lindi Roberts, Carolyn Williamson, Jo Ann S. Passmore, Koleka Mlisana, Francesca Little, Lisa M Bebell, Gerhard Walzl, Melissarose AbrahamsAbstract:In sub-Saharan Africa, which has the highest prevalence of human immunodeficiency virus type 1 (HIV-1) worldwide, most new infections occur by sexual transmission to women [1]. The Genital mucosa is the initial site of viral replication following vaginal transmission of HIV-1 in women and simian immunodeficiency virus (SIV) in rhesus macaques [2, 3]. In macaques, vaginal inoculation with SIV is followed by proinflammatory cytokine production and recruitment of CD4+ T cells that are necessary for local viral expansion and dissemination to the systemic compartment [4–6]. Proinflammatory cytokine expression in the Genital mucosa correlates with viral replication and approaches baseline as peak SIV viremia declines [6]. HIV-1 infection may likewise be accompanied by an early inflammatory cascade in the Genital Tract that is associated with viral replication in this compartment. HIV-1 has been shown to directly induce inflammatory cytokine production via Toll-like receptor 7 and 8 activation [7]. Elevated concentrations of inflammatory cytokines in turn may upregulate HIV-1 replication by recruiting and activating target cells and through NF-κB activation [4, 8–11]. Several studies have shown that cervicovaginal proinflammatory cytokines are upregulated in women with early or chronic HIV-1 infection compared with HIV-uninfected women [10, 12–16]. However this upregulation may be attributed to the high frequency of sexually transmitted infections (STIs) or bacterial vaginosis (BV) in these individuals rather than HIV-1 itself [17]. For example, BV was associated with increased concentrations of proinflammatory interleukin (IL)–1β, whereas chronic HIV-1 infection was not [18]. HIV-1 shedding, which is associated with STIs [19], may induce further inflammatory cytokine production. Plasma cytokine concentrations during early HIV-1 infection are predictive of plasma viral load set points and CD4 depletion [20], and treatment with cytokines such as IL-12p70 and IL-15 during acute SIV infection is associated with altered disease course in macaques [21–23]. Several studies have suggested that cytokine responses in the Genital Tract during the early stages of HIV-1 infection may likewise be associated with disease progression. In macaques, induction of inflammatory cytokines and immune cell influx into the Genital Tract prior to vaginal SIV inoculation was associated with increased plasma viral load set points [24]. This suggests that preexisting Genital Inflammation in humans may similarly influence HIV-1 disease progression. Zara et al [14] demonstrated that upregulation of IL-1β in the Genital Tracts of HIV-1–infected women was associated with increased plasma viral loads. Recently, we reported that elevated proinflammatory cytokines in cervicovaginal lavage (CVL) correlated with lower blood CD4+ T-cell counts during early HIV-1 infection [15]. In this study, the relationships between Genital cytokine concentrations during early HIV-1 infection and plasma viral load set point and blood CD4+ T-cell counts 12 months postinfection were investigated.
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Symptomatic vaginal discharge is a poor predictor of sexually transmitted infections and Genital Tract Inflammation in high-risk women in South Africa
Journal of Infectious Diseases, 2012Co-Authors: Koleka Mlisana, Nivashnee Naicker, Lise Werner, Lindi Roberts, Francois Van Loggerenberg, A. Willem Sturm, Anneke C. Grobler, Cheryl Baxter, Jo Ann S. Passmore, Carolyn WilliamsonAbstract:BACKGROUND: Diagnosis and treatment of sexually transmitted infections (STIs) is a public health priority, particularly in regions where the incidence of human immunodeficiency virus (HIV) infection is high. In most developing countries, STIs are managed syndromically. We assessed the adequacy of syndromic diagnosis of STIs, compared with laboratory diagnosis of STIs, and evaluated the association between STI diagnosis and the risk of HIV acquisition in a cohort of high-risk women.\n\nMETHODS: HIV-uninfected high-risk women (n = 242) were followed for 24 months. Symptoms of STIs were recorded, and laboratory diagnosis of common STI pathogens was conducted every 6 months. Forty-two cytokines were measured by Luminex in cervicovaginal lavage specimens at enrollment. Human immunodeficiency virus type 1 (HIV-1) infection was evaluated monthly.\n\nRESULTS: Only 12.3% of women (25 of 204) who had a laboratory-diagnosed, discharge-causing STI had clinically evident discharge. Vaginal discharge was thus a poor predictor of laboratory-diagnosed STIs (sensitivity, 12.3%; specificity, 93.8%). Cervicovaginal cytokine concentrations did not differ between women with asymptomatic STIs and those with symptomatic STIs and were elevated in women with asymptomatic STIs, compared with women with no STIs or bacterial vaginosis. Although laboratory-diagnosed STIs were associated with increased risk of HIV infection (hazard ratio, 3.3 [95% confidence interval, 1.5-7.2)], clinical symptoms were not.\n\nCONCLUSIONS: Syndromic STI diagnosis dependent on vaginal discharge was poorly predictive of laboratory-diagnosed STI. Laboratory-diagnosed STIs were associated with increased susceptibility to HIV acquisition, while vaginal discharge was not.
Lindi Masson - One of the best experts on this subject based on the ideXlab platform.
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female Genital Tract Inflammation hiv co infection and persistent mucosal human papillomavirus hpv infections
Virology, 2016Co-Authors: Jeanmari Kriek, Shaun L Barnabas, Shameem Z Jaumdally, Lindi Masson, Francesca Little, Zizipho Z A Mbulawa, Pamela P Gumbi, Jennifer Moodley, Lynette Denny, David CoetzeeAbstract:AbsTract Background Persistent Genital infections with high-risk HPV types increase risk of cervical disease and cancer. Since Genital Inflammation increases HIV acquisition risk and cancer progression, we evaluated whether HPV infection induces cytokine expression in the reproductive Tract. Methods Genital cytokines concentrations were measured in 93 HIV-infected and 72 uninfected women. HPV typing was done by Roche Linear array. Persistence and clearance of HPV were evaluated using longitudinal data. Results Infection with HPV did not influence Genital cytokine concentrations. In contrast, HIV-infected women had higher IL-1α, IL-6, IL-8, IP-10, MCP-1 and G-CSF concentrations compared to HIV-uninfected women, and HPV-infections that were more prevalent, persistent and multi-type. Conclusion HPV did not influence inflammatory cytokine levels in the Genital Tract, although immune suppression may favor persistence.
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defining Genital Tract cytokine signatures of sexually transmitted infections and bacterial vaginosis in women at high risk of hiv infection a cross sectional study
Sexually Transmitted Infections, 2014Co-Authors: Lise Werner, Koleka Mlisana, Nonhlanhla N Mkhize, Lindi Masson, Francesca Little, Katharina RonacherAbstract:Objectives Sexually transmitted infections (STI) and bacterial vaginosis (BV) cause female Genital Tract Inflammation. This Inflammation, which is often present in the absence of symptoms, is associated with increased susceptibility to HIV infection. We aimed to evaluate Genital cytokine profiles and the degree of Inflammation associated with common STIs and BV. Methods HIV-uninfected women (n=227) were screened for BV, Chlamydia trachomatis , Neisseria gonorrhoeae , Herpes simplex virus type 2 (HSV-2), and Trichomonas vaginalis . Concentrations of 42 cytokines in cervicovaginal lavages and 13 cytokines in plasma were measured using Luminex. Changes in cytokine profiles were evaluated using Mann–Whitney U test, logistic regression and factor analysis. p Values were adjusted for multiple comparisons using a false discovery rate step-down procedure. Results Women with chlamydia or gonorrhoea had the highest Genital cytokine concentrations, with 17/42 and 14/42 cytokines upregulated compared with women with no infection, respectively. BV was associated with elevated proinflammatory cytokine concentrations, but lower chemokine and haematopoietic cytokine concentrations. HSV-2 reactivation was associated with lower levels of Inflammation, while trichomoniasis did not cause significant differences in Genital cytokine concentrations. Genital infections did not influence plasma cytokine concentrations. Although certain STIs, in particular chlamydia and gonorrhoea, were associated with high Genital cytokine concentrations, only 19% of women with an STI/BV had clinical signs. Conclusions Chlamydia was associated with the highest Genital cytokine levels, followed by gonorrhoea, HSV-2, trichomoniasis, and BV. In regions where HIV is prevalent and STIs are managed syndromically, better STI/BV screening is urgently needed, as certain infections were found to be highly inflammatory.