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1 macaques have a cyclical pattern of changing cervicovaginal Ab and immunoglobulin levels that is simi
4 ted atazanavir (ATV) underwent serial paired cervicovaginal and plasma sampling for antiretroviral co
5 p cultures of human tonsils, lymph nodes and cervicovaginal and rectosigmoid tissues, including proto
6 screened for cervicovaginal HSV-2 DNA, GUD, cervicovaginal and systemic HIV-1 RNA, and reproductive
7 collected daily genital swabs of the vulvar, cervicovaginal, and perianal areas for HSV culture, main
9 different HPV serotypes induced 10-fold more cervicovaginal antigen-specific CD8+ T cells than primin
11 virions initially bind preferentially to the cervicovaginal basement membrane (BM) at sites of trauma
12 atforms for inducing durable intraepithelial cervicovaginal CD8+ T cell responses by promoting local
13 ectively, were cloned and characterized from cervicovaginal cells by use of an overlapping PCR method
17 to gonococcal infection in a murine model of cervicovaginal colonization and identified MisR-regulate
18 ssue drug exposure through modulation of the cervicovaginal, colorectal, or immune cell transporters.
19 cases, the frequency of this response in the cervicovaginal compartment far exceeded the frequency in
21 well as results from in vitro activation of cervicovaginal epithelial cells and U1/HIV promonocytic
23 bitory effect of DES was transient, and most cervicovaginal epithelial cells recovered expression of
24 and that conditioned medium from GC-exposed cervicovaginal epithelial cells with elevated levels of
29 ar cell-associated blood HIV-1 DNA load, and cervicovaginal fluid (CVF) HIV-1 DNA load were determine
31 Appropriate clinical sampling devices for cervicovaginal fluid collection would help physicians de
32 ed to develop an effective device to collect cervicovaginal fluid from women with symptoms of endomet
35 llected for measuring the HIV-1 RNA level in cervicovaginal fluid, phosphate-buffered saline containi
43 clovir had little impact on (1) detection of cervicovaginal HIV-1 RNA (risk ratio [RR], 0.96; 95% con
45 0.8-1.2) at day 7 of treatment, (2) the mean cervicovaginal HIV-1 RNA load (-0.06 log(10) copies/mL;
47 16 IgA was associated with sexual behavior, cervicovaginal HPV 16 DNA, and cytological abnormalities
49 evels (continuous and categorical forms) and cervicovaginal HPV infection (due to high-risk HPV or va
50 have been shown to be at increased risk for cervicovaginal HPV infection and CIN, and cervical cance
51 total of 2353 sexually active women for whom cervicovaginal HPV infection status and serum 25-hydroxy
55 The seroprevalences of IgG in women with cervicovaginal HPV16, HPV16-related types, and other HPV
56 nal HIV-1 RNA (RR, 0.70; 95% CI, 0.4-1.2) or cervicovaginal HSV-2 DNA (RR, 0.69; 95% CI, 0.4-1.3), ha
57 c therapy for herpes reduced the quantity of cervicovaginal HSV-2 DNA and slightly improved ulcer hea
58 study was to assess factors associated with cervicovaginal HSV-2 DNA shedding and genital ulcer dise
61 RT is strongly associated with a decrease in cervicovaginal HSV-2 shedding, and the impact was sustai
62 ious diseases; however, its association with cervicovaginal human papillomavirus (HPV) infection has
64 submicromolar range in ex vivo lymphoid and cervicovaginal human tissues and at 3-12 micromol/L in C
67 y concentration required for protection from cervicovaginal infection is comparable to that required
68 e report the development of a mouse model of cervicovaginal infection with HPV16 that recapitulates t
70 oncomitant lower genital-tract infections on cervicovaginal inflammatory cells was assessed in 967 wo
72 votella bivia) were strongly associated with cervicovaginal inflammatory cytokines, but not with alte
73 helium to be columnar (uterine) or squamous (cervicovaginal) is determined by mesenchymal induction d
76 ducted to analyze the presence of HCV RNA in cervicovaginal lavage (CVL) fluid from 71 women (58 HCV/
77 ty (CMI) was evaluated for the first time in cervicovaginal lavage (CVL) fluid from RVVC patients.
78 sence of a heat-stable soluble factor in the cervicovaginal lavage (CVL) fluid of both HIV-infected a
80 ory cytokine concentrations were measured in cervicovaginal lavage (CVL) from 49 women 6, 17, 30, and
81 igned to determine the antiviral activity in cervicovaginal lavage (CVL) samples collected after intr
82 tic cells secreted TNF- alpha in response to cervicovaginal lavage (CVL) samples from women with BV.
83 ng into the genital tract, paired plasma and cervicovaginal lavage (CVL) samples were obtained from 1
85 nerella vaginalis, and Mycoplasma hominis in cervicovaginal lavage (CVL) samples were quantified by p
87 pothesis-generating study, 17 women provided cervicovaginal lavage (CVL) specimens at baseline (all h
88 irus (CMV) was studied in blood, saliva, and cervicovaginal lavage (CVL) specimens from 33 HIV-1-infe
90 formalin-fixed-tissue specimens collected by cervicovaginal lavage (CVL) within 90 days of each other
92 ysis of 16S ribosomal RNA gene sequencing of cervicovaginal lavage clustered each participant visit i
93 in plasma, female reproductive tract tissue, cervicovaginal lavage fluid and its intracellular metabo
95 rrent quantified HIV-1 RNA concentrations in cervicovaginal lavage fluid in 301 women infected with t
97 p160-specific IgA responses were detected in cervicovaginal lavage fluids in 6 of 13 HEPS CSWs but 0
98 nd prevalence of human papillomavirus DNA in cervicovaginal lavage fluids were all >50% and were 2-30
99 endocervical swabs were more sensitive than cervicovaginal lavage for HIV-1 RNA detection by PCR but
102 s and proviral DNA in cervical, vaginal, and cervicovaginal lavage samples by polymerase chain reacti
104 nerella vaginalis, and Mycoplasma hominis in cervicovaginal lavage samples were quantified by PCR.
110 al neoplasia grade 3 and cancer (CIN3+) with cervicovaginal lavage specimens collected at enrollment
112 NA testing were conducted annually in serial cervicovaginal lavage specimens obtained over 8-10 years
113 land (of whom 184 were HIV+), provided 1,426 cervicovaginal lavage specimens tested for HPV DNA by a
119 w ProTalpha variants from CD8(+) T cells and cervicovaginal lavage with potent anti-HIV-1 activity.
120 Schistosoma PCR was done on urine, biopsy, cervicovaginal lavage, and genital mucosal surface speci
122 wicks should be considered as an adjunct to cervicovaginal lavage, to improve the sensitivity and pr
123 py and tests for human papillomavirus DNA in cervicovaginal lavage-for a median follow-up of 3.2 year
126 t lifestyle and sexual behavior and obtained cervicovaginal-lavage samples for the detection of HPV D
127 y, and inflammatory cells were quantified in cervicovaginal lavages (CVLs) of 24 women enrolled in th
129 L-10 were measured prior to HIV infection in cervicovaginal lavages from 58 HIV seroconverters and 58
130 tryptophan, indole, and IFN-gamma levels in cervicovaginal lavages from women with either naturally
132 munoglobulins G and A and some antibodies in cervicovaginal lavages varied with the stages of the men
133 ADCC mediated by antibodies present in sera, cervicovaginal lavages, and breast milk from HIV-1-infec
134 blot analysis, secreted HD-5 was detected in cervicovaginal lavages, with the highest concentrations
137 These studies suggest that members of the cervicovaginal microbiome can modify N. gonorrhoeae, whi
139 Our study proposes a mechanism by which cervicovaginal microbiota impact genital inflammation an
142 is consistent with hypotheses that the local cervicovaginal milieu plays a role in susceptibility to
143 ed CD8+ T cell responses in the female mouse cervicovaginal mucosa after intravaginal immunization wi
144 duction of innate antiviral responses in the cervicovaginal mucosa by topical application of TLR agon
147 Soluble factors from CD8(+) T cells and cervicovaginal mucosa of women are recognized as importa
149 ts for SIV were in the lamina propria of the cervicovaginal mucosa, immediately subjacent to the epit
150 ss the HIV-1 coreceptor CCR5 in normal human cervicovaginal mucosa, whereas all three cell types expr
153 fibers (pore sizes) in fresh undiluted human cervicovaginal mucus (CVM) obtained from volunteers with
155 tibodies (Ab) can trap individual virions in cervicovaginal mucus (CVM), thereby reducing infection i
158 (PLGA) nanoparticles rapidly penetrate human cervicovaginal mucus, whereas PLGA nanoparticles coated
164 tration and viscoelastic properties of these cervicovaginal samples are similar to those in many othe
165 ith suppressed plasma virus loads, blood and cervicovaginal samples collected twice weekly for 3 week
166 ction by cervical cytology and self-obtained cervicovaginal samples for up to 27 months, and for vacc
170 nce of human immunodeficiency virus (HIV) in cervicovaginal secretions (CVS) may be a risk factor for
173 nuclear cells and SIV-specific antibodies in cervicovaginal secretions at the time of challenge was a
177 specific antibodies were not detected in the cervicovaginal secretions of 10 STV monkeys examined.
178 ections have levels of sialidases present in cervicovaginal secretions that can result in desialylati
179 e cervix and assays for fetal fibronectin in cervicovaginal secretions, also had low sensitivity and
180 ysis of molecular and cellular components in cervicovaginal secretions, as well as results from in vi
181 ular, as well as other bodily fluids such as cervicovaginal secretions, could increase oral transmiss
182 IgA and IgG Abs in mucosal secretions (e.g., cervicovaginal secretions, rectal washes, and saliva) an
186 ews; physical examination; blood, urine, and cervicovaginal specimen collection and repository; labor
188 tween clinician-collected and self-collected cervicovaginal specimens (P > 0.01 for all comparisons).
189 zed HPV DNA types detected in self-collected cervicovaginal specimens and demographic, sexual behavio
190 ecovered throughout the 8-week experiment in cervicovaginal specimens and up to 2 weeks postinfection
191 ssays by each method were performed with 596 cervicovaginal specimens collected from participants in
192 d HSV-2 present in more than 60,000 clinical cervicovaginal specimens derived from samples originatin
194 eptible leukocytes on female genital mucosa, cervicovaginal specimens from 32 HIV-negative STD clinic
196 of carcinogenic human papillomavirus DNA in cervicovaginal specimens self-collected using a novel de
198 cted cervical specimens, clinician-collected cervicovaginal specimens, and self-collected cervicovagi
200 determined by the Linear Array HPV Assay in cervicovaginal swab samples from females aged 14-59 year
202 dida species-specific PCR tests performed on cervicovaginal swabs over a 4-year period demonstrated c
206 cells and macrophages in vitro, in polarized cervicovaginal tissue explants, and in the female genita
207 by examining mononuclear cells obtained from cervicovaginal tissue, the mechanisms whereby HIV type 1
210 osal barrier greatly limits the infection of cervicovaginal tissues, and thus the initial founder pop
211 els of GBS interaction with the human female cervicovaginal tract using human vaginal and cervical ep
212 ces of the respiratory, gastrointestinal and cervicovaginal tracts to efficiently reach the underlyin
213 mucosal surfaces of the gastrointestinal and cervicovaginal tracts, both of which are normally coated
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