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1 e for a role for IFI16 in protection against genital herpes.
2 quisition among patients with newly acquired genital herpes.
3 kin-lesion biopsy samples from subjects with genital herpes.
4 by showing that CVL samples prevented murine genital herpes.
5 inoculation was examined in a mouse model of genital herpes.
6 also become commonly associated with primary genital herpes.
7 d monthly for clinical signs and symptoms of genital herpes.
8 the reduction in transmission of symptomatic genital herpes.
9 ritical in developing effective vaccines for genital herpes.
10 rce (USPSTF) recommendation on screening for genital herpes.
11 counseling the patient with newly diagnosed genital herpes.
12 ans is vital for improving the management of genital herpes.
13 tic vaccine would help control the spread of genital herpes.
14 ns (84.7%) had never received a diagnosis of genital herpes.
15 ose regular sexual partners had a history of genital herpes.
16 ts and providers about care of patients with genital herpes.
17 was evaluated using the guinea pig model of genital herpes.
18 viral therapies for the control of recurrent genital herpes.
19 nto a candidate vaccine strain for HSV-2 and genital herpes.
20 even in subjects with no reported history of genital herpes.
21 ccinated persons who did and did not develop genital herpes.
22 well tolerated for suppression of recurrent genital herpes.
23 equire suppressive therapy for management of genital herpes.
24 ted in animal models of recurrent ocular and genital herpes.
25 bility is central to preventing and treating genital herpes.
26 on, and their reactivation leads to oral and genital herpes.
27 n adjuvant failed to show protection against genital herpes.
28 coprotein D (gD2) subunit vaccine to prevent genital herpes.
29 nner in otherwise healthy men and women with genital herpes.
30 ng potentiates the susceptibility of mice to genital herpes.
31 ht new strategies for vaccine design against genital herpes.
32 n the progesterone-induced B6 mouse model of genital herpes.
33 , including HSV type 2 (HSV-2), which causes genital herpes.
34 atic" vaccine against ocular, orofacial, and genital herpes.
35 tions for treatment of episodes of recurrent genital herpes.
36 of ASP2151 for episodic therapy of recurrent genital herpes.
37 ype 2 infection in mice and earlier onset of genital herpes.
38 s is an uncommon but serious complication of genital herpes.
41 ) 57 women at 70 clinic visits with clinical genital herpes; (2) 39 of the same women at 46 clinic vi
42 follow-up visit: trichomoniasis in 23 (18%); genital herpes, 20 (12%); gonorrhea, 9 (7%); syphilis, 7
43 roid, 29% had syphilitic ulcers, and 10% had genital herpes; 32% of the ulcer specimens were M-PCR ne
44 e 53 subjects who had no reported history of genital herpes, 33 (62 percent) subsequently reported ha
46 oniasis in 16 women (11%); syphilis, 9 (6%); genital herpes, 8 (6%); gonorrhea, 5 (4%); chlamydia, 5
47 ce partners were followed for recurrences of genital herpes; 89 were enrolled in a substudy of HSV-2
48 common as HSV-2 in causing first episodes of genital herpes, a disease that is associated with an inc
49 and B vaccine in the treatment of recurrent genital herpes, a randomized, placebo-controlled trial w
50 ls of protection against acute and recurrent genital herpes after vaginal challenge with wild-type vi
51 ficantly reduces the risk of transmission of genital herpes among heterosexual, HSV-2-discordant coup
54 afforded by gD2/AS04 against HSV-1 and HSV-2 genital herpes and investigated whether immunization cou
55 ex virus type 2 (HSV-2) is the cause of most genital herpes and is almost always sexually transmitted
57 be aware of the subclinical presentation of genital herpes and the potential these patients have for
58 rat may provide an excellent model to study genital herpes and to evaluate preventive strategies.
59 d 11 with HSV-2 antibodies but no history of genital herpes) and obtained daily swabs for viral cultu
61 ects (72 percent) who reported no history of genital herpes, and HSV DNA was detected by the polymera
63 HSV-2 but who reported having no history of genital herpes, and we compared their patterns of viral
64 The frequency of viral shedding in men with genital herpes appears comparable with that in women.
65 study, 52 patients with frequently recurrent genital herpes applied topical resiquimod gel 0.01% (twi
68 monitored couples, most persons who transmit genital herpes are not aware of having the infection.
69 of subjects who did not have a recurrence of genital herpes at 6 months was 65% among valacyclovir re
70 ur HSV-2-seropositive women with symptomatic genital herpes attended a clinic daily during a 30-day p
71 c interaction between HIV-1 transmission and genital herpes being of special concern for control of b
73 microbicide and/or therapeutic agent against genital herpes by increasing resistance to HSV-2 and enh
75 cubation period and most persons who acquire genital herpes can identify the transmitting partner, a
80 pDCs are critical in innate defense against genital herpes challenge, adaptive Th1 immunity develope
82 ACIDFORM protected 21 (81%) of 26 mice from genital herpes, compared with 3 (12%) of 25 mice who rec
83 pants whose partners disclosed that they had genital herpes, compared with participants whose partner
85 anatomical locations may be responsible for genital herpes control in chronically infected individua
87 women were classified into 3 groups based on genital herpes diagnosis and treatment: genital herpes w
89 The primary end point was the occurrence of genital herpes disease in all subjects in Study 1 and in
90 lum and monophosphoryl lipid A (MPL) reduced genital herpes disease in HSV-1-seronegative women but n
92 ationships between these cells and recurrent genital herpes disease severity in the general populatio
95 irus titers; 3) had decreased overt signs of genital herpes disease; and 4) did not succumb to lethal
96 pared with being unexposed, having untreated genital herpes during first or second trimester was asso
99 ns from 118 patients with culture-documented genital herpes episodes, and their results were compared
100 n may influence the epidemiology of clinical genital herpes, even if prior HSV-1 infection does not p
101 and 14 were given an incorrect diagnosis of genital herpes, for a ratio of true positive results to
105 infections (STI), but diagnostic methods for genital herpes have not kept pace with the movement towa
107 as vaginalis infection, primary or recurrent genital herpes, having bacterial vaginosis by Nugent cri
109 Fourteen of 15 mice were protected from genital herpes if they were challenged with HSV-2 pretre
110 rcentage reported having been diagnosed with genital herpes in 1999-2004 compared with 1988-1994 (1.8
111 1 genital herpes was less than that of HSV-2 genital herpes in cotton rats, and yet the model allowed
115 translated to significant protection against genital herpes in mice treated with 0.1% griffithsin gel
118 her efficacy against HSV-1 compared to HSV-2 genital herpes in the novel DMPA-synchronized cotton rat
120 glycoprotein D vaccine has efficacy against genital herpes in women who are seronegative for both HS
121 ncreasing evidence that sexually transmitted genital herpes increases HIV acquisition, and the reacti
124 to estimate the prevalence and incidence of genital herpes infection and to assess the relation betw
125 vealed increased risk of PTD associated with genital herpes infection if left untreated and a potenti
126 d effective for the suppression of recurrent genital herpes infection in HIV-infected individuals.
127 ulcers caused by HSV-2, which suggests that genital herpes infection likely increases the efficiency
130 poly I:C has been shown to protect mice from genital herpes infection, the mechanism by which these a
133 (endocervix and ectocervix/vagina) to mimic genital herpes infections caused by herpes simplex virus
134 ntibody can provide passive immunity against genital herpes infections in mice; orally administered p
137 simplex virus 1 (HSV-1), a leading cause of genital herpes, infects oral or genital mucosal epitheli
139 s to HSV-2 of 22% in the general population, genital herpes is 1 of the 3 most prevalent sexually tra
143 sions and Relevance: Serologic screening for genital herpes is associated with a high rate of false-p
145 entral issue in the public health problem of genital herpes is the high proportion of genital HSV inf
148 , the principal causative agent of recurrent genital herpes, is a highly prevalent viral infection wo
151 elivery, the standard of care for women with genital herpes lesions at the time of delivery, reduces
153 -2 gD2 antigen protected guinea pigs against genital herpes, limiting primary infection and reducing
154 interventions more specifically tailored to genital herpes may be useful and should be an important
155 DCs in the skin during primary or recurrent genital herpes may enhance HIV-1 infection of adjacent D
158 ositive for HSV-2 only reported a history of genital herpes more frequently (16.2%) than persons sero
160 ies suggest that most sexual transmission of genital herpes occurs when persons shed virus but lack l
161 rica have measured the unfavorable effect of genital herpes on infected patients, health care resourc
164 hough HSV-2 remained the predominant type of genital herpes, over the 6-year span of this study, ther
166 in the prevalence of Incurable STDs (such as genital herpes); perhaps greater Importance of symptomat
167 ects with no prior history of oral/labial or genital herpes possessed HSV-specific T cell immunity bu
173 g a partner who disclosed that he or she had genital herpes remained a strong protective factor again
182 he efficacy of valacyclovir and acyclovir on genital herpes simplex virus (HSV) shedding was assessed
183 Attempts to develop a vaccine to prevent genital herpes simplex virus 2 (HSV-2) disease have been
185 e epidemiological studies have reported that genital herpes simplex virus 2 (HSV-2) infection increas
186 study assessed 79 men (63 with a history of genital herpes simplex virus [HSV] type 2 infection, 5 w
188 wice daily) for the suppression of recurrent genital herpes simplex virus infections in human immunod
190 icient (CXCL10(-/-)) mice which succumbed to genital herpes simplex virus type 2 (HSV-2) infection an
192 min) relative to host immune defense against genital herpes simplex virus type 2 (HSV-2) infection ha
193 investigated the mechanism of resistance to genital herpes simplex virus type 2 (HSV-2) infection in
194 Clinical and virologic manifestations of genital herpes simplex virus type 2 (HSV-2) infection va
195 e vaccines are effective in animal models of genital herpes simplex virus type 2 (HSV-2) infection.
196 n = 188) from 29 patients with first-episode genital herpes simplex virus type 2 (HSV-2) infections w
198 persons without past or current symptoms of genital herpes; studies evaluating accuracy and harms of
199 ter adjustment for sex, HSV type 1, oral and genital herpes symptoms, immigrant status, and the inter
200 ns with laboratory-documented newly acquired genital herpes, the median duration of the sexual relati
202 mptomatic but nevertheless fail to recognize genital herpes; they serve as reservoirs for transmissio
204 156 HSV-2-positive persons with a history of genital herpes to receive one of four doses of oral prit
205 gnancy events, including vaginal infections, genital herpes, urinary tract infections (UTIs), and oth
207 olunteers entering trials of investigational genital herpes vaccines, 6 of the 24 immunocompetent sub
208 inical diagnosis of syphilis, chancroid, and genital herpes was 93%, 53%, and 0% and specificity was
210 of valaciclovir for suppression of recurrent genital herpes was conducted among 1479 immunocompetent
212 for bacterial vaginosis, trichomoniasis, and genital herpes was performed in a high-prevalence popula
213 in the subjects with no reported history of genital herpes was similar to that in the subjects with
214 tage who reported having been diagnosed with genital herpes was statistically different (14.3% in 199
219 plex virus 2 (HSV-2) is the primary cause of genital herpes, which is one of the most common sexually
220 treatment: genital herpes without treatment, genital herpes with antiherpes treatment, and no herpes
221 d on genital herpes diagnosis and treatment: genital herpes without treatment, genital herpes with an
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