scholarly journals Nosocomial Infection Among Children With Symptomatic Human Immunodeficiency Virus Infection

2002 ◽  
Vol 23 (11) ◽  
pp. 689-692 ◽  
Author(s):  
Ana Cristina Cisne Frota ◽  
Rosana Maria Rangel Santos ◽  
Thalita Fernandes Abreu ◽  
Enaldo Góes Silva ◽  
Carmem Lúcia Pessoa-Silva

AbstractA prospective cohort study was conducted during a 15-month period to compare nosocomial infections (NIs) among pediatric patients without (n = 989) and with (n = 50) symptomatic human immunodeficiency virus (HIV) infection. Patients with symptomatic HIV infection presented higher overall NI incidence density rates (relative risk, 1.65; P = .0001), and may represent a population at high risk for the acquisition of NI.

1989 ◽  
Vol 82 (7) ◽  
pp. 825-828
Author(s):  
MICHAEL K. LINDSAY ◽  
HERBERT B. PETERSON ◽  
DAVID C. MUNDY ◽  
BARBARA A. SLADE ◽  
TERRY FENG ◽  
...  

PEDIATRICS ◽  
1993 ◽  
Vol 91 (1) ◽  
pp. 39-44
Author(s):  
George A. Gellert ◽  
Michael J. Durfee ◽  
Carol D. Berkowitz ◽  
Kathleen V. Higgins ◽  
Vincent C. Tubiolo

This study assessed the situational and sociodemographic characteristics of children infected with human immunodeficiency virus (HIV) from pediatric sexual abuse. A letter of inquiry was sent to 2147 professionals across health and social service disciplines involved with child abuse assessment, treatment, and prevention. Respondents working in programs where HIV antibody testing of abuse victims occurs and who had identified HIV infection in one or more abused children were sent a survey to assess the demographics of victims, the family/living situation where abuse occurred, alternative risks for HIV infection, bases for diagnosis of sexual abuse and for HIV antibody testing, and profiles of the perpetrator and type of abuse. Of 5622 estimated HIV antibody tests conducted during 113 198 sex abuse assessments, 28 children were infected with HIV and lacked any alternative transmission route to that of sexual abuse. A total of 41 HIV-infected children with a history of sexual abuse were identified. Thirteen cases had alternative risk factors and were excluded from analysis. Sixty-four percent of the 28 victims with sexual abuse as the sole risk factor were female and 71% were African-American. The mean age was 9 years. Coinfection with another sexually transmitted disease (STD) occurred in 9 (33%) cases. Sexual abuse was diagnosed on the basis of a victim disclosure in 21 (75%) cases. The basis for HIV antibody testing was physical findings suggestive of HIV infection in 9 (32%) cases, HIV-seropositive or high-risk perpetrator in 6 (21%) and 2 (7%) cases, respectively, and the presence of another STD in the victim in 4 (14%) cases. Perpetrators were a child's parent in 10 (42%) cases and another relative in 6 (25%) cases. Perpetrators had behavioral risk factors for or signs/symptoms of HIV infection in 14 (58%) cases. The serostatus of perpetrators was known at time of abuse assessment in 16 (67%) cases and all were seropositive. Duration and form of abusive acts were variable, with 3 victims reporting a single episode and 13 (68%) reporting 6 or more episodes. Penile vaginal and/or rectal penetration was reported in only 50% of cases. It is concluded that sexual abuse must be considered as a potential, although infrequent, mode of transmission of HIV infection in children. Children who have been abused should be evaluated selectively for HIV infection particularly if the perpetrator is known to be HIV seropositive or engages in HIV high-risk behavior, if abuse occurred in a geographic area of high disease prevalence, and if the child has symptoms of HIV infection or another STD. Children who are found to be HIV infected and lack risk factors such as prior transfusion or maternal (perinatal) infection should be assessed for pediatric sexual abuse.


Open Biology ◽  
2021 ◽  
Vol 11 (11) ◽  
Author(s):  
Mahmoud Mohammad Yaseen ◽  
Nizar Mohammad Abuharfeil ◽  
Homa Darmani

There are several mechanisms by which human immunodeficiency virus (HIV) can mediate immune dysfunction and exhaustion during the course of infection. Chronic immune activation, after HIV infection, seems to be a key driving force of such unwanted consequences, which in turn worsens the pathological status. In such cases, the immune system is programmed to initiate responses that counteract unwanted immune activation, for example through the expansion of myeloid-derived suppressor cells (MDSCs). Although the expansion of immune suppressor cells in the setting of systemic chronic immune activation, in theory, is expected to contain immune activation, HIV infection is still associated with a remarkably high level of biomarkers of immune activation. Paradoxically, the expansion of immune suppressor cells during HIV infection can suppress potent anti-viral immune responses, which in turn contribute to viral persistence and disease progression. This indicates that HIV hijacks not only immune activation but also the immune regulatory responses to its advantage. In this work, we aim to pave the way to comprehend how such unwanted expansion of MDSCs could participate in the pathology of acute/primary and chronic HIV infection in humans, as well as simian immunodeficiency virus infection in rhesus macaques, according to the available literature.


1987 ◽  
Vol 126 (4) ◽  
pp. 568-575 ◽  
Author(s):  
JOAN S. CHMIEL ◽  
ROGER DETELS ◽  
RICHARD A. KASLOW ◽  
MARK VAN RADEN ◽  
LAWRENCE A. KINGSLEY ◽  
...  

2007 ◽  
Vol 14 (9) ◽  
pp. 1102-1107 ◽  
Author(s):  
Richard M. Novak ◽  
Betty A. Donoval ◽  
Parrie J. Graham ◽  
Lucy A. Boksa ◽  
Gregory Spear ◽  
...  

ABSTRACT Innate immune factors in mucosal secretions may influence human immunodeficiency virus type 1 (HIV-1) transmission. This study examined the levels of three such factors, genital tract lactoferrin [Lf], secretory leukocyte protease inhibitor [SLPI], and RANTES, in women at risk for acquiring HIV infection, as well as cofactors that may be associated with their presence. Women at high risk for HIV infection meeting established criteria (n = 62) and low-risk controls (n = 33) underwent cervicovaginal lavage (CVL), and the CVL fluid samples were assayed for Lf and SLPI. Subsets of 26 and 10 samples, respectively, were assayed for RANTES. Coexisting sexually transmitted infections and vaginoses were also assessed, and detailed behavioral information was collected. Lf levels were higher in high-risk (mean, 204 ng/ml) versus low-risk (mean, 160 ng/ml, P = 0.007) women, but SLPI levels did not differ, and RANTES levels were higher in only the highest-risk subset. Lf was positively associated only with the presence of leukocytes in the CVL fluid (P < 0.0001). SLPI levels were lower in women with bacterial vaginosis [BV] than in those without BV (P = 0.04). Treatment of BV reduced RANTES levels (P = 0.05). The influence, if any, of these three cofactors on HIV transmission in women cannot be determined from this study. The higher Lf concentrations observed in high-risk women were strongly associated with the presence of leukocytes, suggesting a leukocyte source and consistent with greater genital tract inflammation in the high-risk group. Reduced SLPI levels during BV infection are consistent with an increased risk of HIV infection, which has been associated with BV. However, the increased RANTES levels in a higher-risk subset of high-risk women were reduced after BV treatment.


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