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1 ype 2 infection in mice and earlier onset of genital herpes.
2 s is an uncommon but serious complication of genital herpes.
3 quisition among patients with newly acquired genital herpes.
4 kin-lesion biopsy samples from subjects with genital herpes.
5 by showing that CVL samples prevented murine genital herpes.
6 ced significant protection against recurrent genital herpes.
7 inoculation was examined in a mouse model of genital herpes.
8 also become commonly associated with primary genital herpes.
9 d monthly for clinical signs and symptoms of genital herpes.
10 the reduction in transmission of symptomatic genital herpes.
11 e for a role for IFI16 in protection against genital herpes.
12 ritical in developing effective vaccines for genital herpes.
13 counseling the patient with newly diagnosed genital herpes.
14 ans is vital for improving the management of genital herpes.
15 tic vaccine would help control the spread of genital herpes.
16 ns (84.7%) had never received a diagnosis of genital herpes.
17 ose regular sexual partners had a history of genital herpes.
18 ts and providers about care of patients with genital herpes.
19 was evaluated using the guinea pig model of genital herpes.
20 viral therapies for the control of recurrent genital herpes.
21 nto a candidate vaccine strain for HSV-2 and genital herpes.
22 even in subjects with no reported history of genital herpes.
23 ccinated persons who did and did not develop genital herpes.
24 well tolerated for suppression of recurrent genital herpes.
25 equire suppressive therapy for management of genital herpes.
26 ted in animal models of recurrent ocular and genital herpes.
27 sma genitalium, and no cure is available for genital herpes.
28 No cure is available for genital herpes.
29 ll therapeutic vaccine strategy in combating genital herpes.
30 , Mycoplasma genitalium, trichomoniasis, and genital herpes.
31 reduced frequency and severity of recurrent genital herpes.
32 individuals aged 15 to 49 years, living with genital herpes.
33 ased the severity and frequency of recurrent genital herpes.
34 rce (USPSTF) recommendation on screening for genital herpes.
35 bility is central to preventing and treating genital herpes.
36 on, and their reactivation leads to oral and genital herpes.
37 n adjuvant failed to show protection against genital herpes.
38 coprotein D (gD2) subunit vaccine to prevent genital herpes.
39 nner in otherwise healthy men and women with genital herpes.
40 ng potentiates the susceptibility of mice to genital herpes.
41 ht new strategies for vaccine design against genital herpes.
42 n the progesterone-induced B6 mouse model of genital herpes.
43 , including HSV type 2 (HSV-2), which causes genital herpes.
44 atic" vaccine against ocular, orofacial, and genital herpes.
45 tions for treatment of episodes of recurrent genital herpes.
46 of ASP2151 for episodic therapy of recurrent genital herpes.
49 ) 57 women at 70 clinic visits with clinical genital herpes; (2) 39 of the same women at 46 clinic vi
50 follow-up visit: trichomoniasis in 23 (18%); genital herpes, 20 (12%); gonorrhea, 9 (7%); syphilis, 7
51 roid, 29% had syphilitic ulcers, and 10% had genital herpes; 32% of the ulcer specimens were M-PCR ne
52 e 53 subjects who had no reported history of genital herpes, 33 (62 percent) subsequently reported ha
54 oniasis in 16 women (11%); syphilis, 9 (6%); genital herpes, 8 (6%); gonorrhea, 5 (4%); chlamydia, 5
55 ce partners were followed for recurrences of genital herpes; 89 were enrolled in a substudy of HSV-2
56 common as HSV-2 in causing first episodes of genital herpes, a disease that is associated with an inc
57 and B vaccine in the treatment of recurrent genital herpes, a randomized, placebo-controlled trial w
58 ls of protection against acute and recurrent genital herpes after vaginal challenge with wild-type vi
59 ficantly reduces the risk of transmission of genital herpes among heterosexual, HSV-2-discordant coup
63 afforded by gD2/AS04 against HSV-1 and HSV-2 genital herpes and investigated whether immunization cou
64 ex virus type 2 (HSV-2) is the cause of most genital herpes and is almost always sexually transmitted
66 e mechanisms of protection against recurrent genital herpes and promote the tegument RR2 protein as a
67 T(RM) cells in protection against recurrent genital herpes and promotes the RR2-based subunit therap
68 e of infection and the severity of recurrent genital herpes and propose the novel prime-pull vaccine
69 s and the VM in protection against recurrent genital herpes and propose the prime-pull therapeutic va
70 be aware of the subclinical presentation of genital herpes and the potential these patients have for
71 rat may provide an excellent model to study genital herpes and to evaluate preventive strategies.
72 d 11 with HSV-2 antibodies but no history of genital herpes) and obtained daily swabs for viral cultu
74 ects (72 percent) who reported no history of genital herpes, and HSV DNA was detected by the polymera
77 HSV-2 but who reported having no history of genital herpes, and we compared their patterns of viral
78 The frequency of viral shedding in men with genital herpes appears comparable with that in women.
79 study, 52 patients with frequently recurrent genital herpes applied topical resiquimod gel 0.01% (twi
82 monitored couples, most persons who transmit genital herpes are not aware of having the infection.
83 of subjects who did not have a recurrence of genital herpes at 6 months was 65% among valacyclovir re
84 ur HSV-2-seropositive women with symptomatic genital herpes attended a clinic daily during a 30-day p
85 c interaction between HIV-1 transmission and genital herpes being of special concern for control of b
87 microbicide and/or therapeutic agent against genital herpes by increasing resistance to HSV-2 and enh
89 cubation period and most persons who acquire genital herpes can identify the transmitting partner, a
91 Africa region, the 3.9 million seroprevalent genital herpes cases from 2020 to 2030 contributed to US
96 pDCs are critical in innate defense against genital herpes challenge, adaptive Th1 immunity develope
98 ACIDFORM protected 21 (81%) of 26 mice from genital herpes, compared with 3 (12%) of 25 mice who rec
99 pants whose partners disclosed that they had genital herpes, compared with participants whose partner
102 anatomical locations may be responsible for genital herpes control in chronically infected individua
104 women were classified into 3 groups based on genital herpes diagnosis and treatment: genital herpes w
105 The primary end point was occurrence of genital herpes disease due to either HSV-1 or HSV-2 from
106 The primary end point was the occurrence of genital herpes disease in all subjects in Study 1 and in
107 lum and monophosphoryl lipid A (MPL) reduced genital herpes disease in HSV-1-seronegative women but n
109 ationships between these cells and recurrent genital herpes disease severity in the general populatio
112 irus titers; 3) had decreased overt signs of genital herpes disease; and 4) did not succumb to lethal
113 pared with being unexposed, having untreated genital herpes during first or second trimester was asso
116 ns from 118 patients with culture-documented genital herpes episodes, and their results were compared
117 n may influence the epidemiology of clinical genital herpes, even if prior HSV-1 infection does not p
118 and 14 were given an incorrect diagnosis of genital herpes, for a ratio of true positive results to
122 le HP inhibitors (HPIs) for the treatment of genital herpes has been hindered by the lack of structur
123 infections (STI), but diagnostic methods for genital herpes have not kept pace with the movement towa
125 as vaginalis infection, primary or recurrent genital herpes, having bacterial vaginosis by Nugent cri
127 Fourteen of 15 mice were protected from genital herpes if they were challenged with HSV-2 pretre
128 accine strategy to protect against recurrent genital herpes.IMPORTANCEThe present study investigates
130 rcentage reported having been diagnosed with genital herpes in 1999-2004 compared with 1988-1994 (1.8
131 d economic and quality-of-life losses due to genital herpes in 2019, in 90 LMICs, and from 2020 to 20
132 1 genital herpes was less than that of HSV-2 genital herpes in cotton rats, and yet the model allowed
138 translated to significant protection against genital herpes in mice treated with 0.1% griffithsin gel
142 her efficacy against HSV-1 compared to HSV-2 genital herpes in the novel DMPA-synchronized cotton rat
143 t on the frequency and severity of recurrent genital herpes in the recurrent herpes guinea pig model.
145 glycoprotein D vaccine has efficacy against genital herpes in women who are seronegative for both HS
146 ncreasing evidence that sexually transmitted genital herpes increases HIV acquisition, and the reacti
149 to estimate the prevalence and incidence of genital herpes infection and to assess the relation betw
150 vealed increased risk of PTD associated with genital herpes infection if left untreated and a potenti
151 d effective for the suppression of recurrent genital herpes infection in HIV-infected individuals.
152 l and pathophysiological features typical of genital herpes infection in humans, including the produc
155 ulcers caused by HSV-2, which suggests that genital herpes infection likely increases the efficiency
157 guidelines, key questions for management of genital herpes infection were developed with a panel of
159 poly I:C has been shown to protect mice from genital herpes infection, the mechanism by which these a
164 (endocervix and ectocervix/vagina) to mimic genital herpes infections caused by herpes simplex virus
165 ntibody can provide passive immunity against genital herpes infections in mice; orally administered p
168 simplex virus 1 (HSV-1), a leading cause of genital herpes, infects oral or genital mucosal epitheli
170 s to HSV-2 of 22% in the general population, genital herpes is 1 of the 3 most prevalent sexually tra
175 sions and Relevance: Serologic screening for genital herpes is associated with a high rate of false-p
177 peutic mucosal vaccines.IMPORTANCE Recurrent genital herpes is one of the most common sexually transm
178 entral issue in the public health problem of genital herpes is the high proportion of genital HSV inf
181 , the principal causative agent of recurrent genital herpes, is a highly prevalent viral infection wo
184 elivery, the standard of care for women with genital herpes lesions at the time of delivery, reduces
187 -2 gD2 antigen protected guinea pigs against genital herpes, limiting primary infection and reducing
188 interventions more specifically tailored to genital herpes may be useful and should be an important
189 DCs in the skin during primary or recurrent genital herpes may enhance HIV-1 infection of adjacent D
192 ositive for HSV-2 only reported a history of genital herpes more frequently (16.2%) than persons sero
194 ies suggest that most sexual transmission of genital herpes occurs when persons shed virus but lack l
195 ficacy, in the guinea pig model of recurrent genital herpes, of subunit vaccine candidates that were
196 ficacy, in the guinea pig model of recurrent genital herpes, of subunit vaccine candidates that were
197 rica have measured the unfavorable effect of genital herpes on infected patients, health care resourc
200 hough HSV-2 remained the predominant type of genital herpes, over the 6-year span of this study, ther
202 in the prevalence of Incurable STDs (such as genital herpes); perhaps greater Importance of symptomat
203 ects with no prior history of oral/labial or genital herpes possessed HSV-specific T cell immunity bu
206 of 145 persons who had the severity of their genital herpes quantified through determination of their
213 g a partner who disclosed that he or she had genital herpes remained a strong protective factor again
223 he efficacy of valacyclovir and acyclovir on genital herpes simplex virus (HSV) shedding was assessed
225 Attempts to develop a vaccine to prevent genital herpes simplex virus 2 (HSV-2) disease have been
227 e epidemiological studies have reported that genital herpes simplex virus 2 (HSV-2) infection increas
228 study assessed 79 men (63 with a history of genital herpes simplex virus [HSV] type 2 infection, 5 w
230 wice daily) for the suppression of recurrent genital herpes simplex virus infections in human immunod
232 icient (CXCL10(-/-)) mice which succumbed to genital herpes simplex virus type 2 (HSV-2) infection an
234 min) relative to host immune defense against genital herpes simplex virus type 2 (HSV-2) infection ha
235 investigated the mechanism of resistance to genital herpes simplex virus type 2 (HSV-2) infection in
236 Clinical and virologic manifestations of genital herpes simplex virus type 2 (HSV-2) infection va
237 e vaccines are effective in animal models of genital herpes simplex virus type 2 (HSV-2) infection.
238 n = 188) from 29 patients with first-episode genital herpes simplex virus type 2 (HSV-2) infections w
244 persons without past or current symptoms of genital herpes; studies evaluating accuracy and harms of
245 ter adjustment for sex, HSV type 1, oral and genital herpes symptoms, immigrant status, and the inter
246 m DRG and reducing the severity of recurrent genital herpes, the mechanisms for recruiting these T ce
247 ns with laboratory-documented newly acquired genital herpes, the median duration of the sexual relati
248 le candidate Ag to be incorporated in future genital herpes therapeutic mucosal vaccines.IMPORTANCE R
250 mptomatic but nevertheless fail to recognize genital herpes; they serve as reservoirs for transmissio
252 156 HSV-2-positive persons with a history of genital herpes to receive one of four doses of oral prit
253 gnancy events, including vaginal infections, genital herpes, urinary tract infections (UTIs), and oth
254 accine strategy to protect against recurrent genital herpes using the latently infected guinea pig mo
256 olunteers entering trials of investigational genital herpes vaccines, 6 of the 24 immunocompetent sub
257 inical diagnosis of syphilis, chancroid, and genital herpes was 93%, 53%, and 0% and specificity was
259 of valaciclovir for suppression of recurrent genital herpes was conducted among 1479 immunocompetent
261 for bacterial vaginosis, trichomoniasis, and genital herpes was performed in a high-prevalence popula
262 in the subjects with no reported history of genital herpes was similar to that in the subjects with
263 tage who reported having been diagnosed with genital herpes was statistically different (14.3% in 199
268 plex virus 2 (HSV-2) is the primary cause of genital herpes, which is one of the most common sexually
269 treatment: genital herpes without treatment, genital herpes with antiherpes treatment, and no herpes
270 d on genital herpes diagnosis and treatment: genital herpes without treatment, genital herpes with an