Publications by authors named "Mariel Jais"
Article Synopsis
- Hormonal changes during the menstrual cycle influence immune responses in the cervicovaginal area, with varying concentrations of immune mediators like cytokines and immunoglobulins across different phases.
- A systematic review and meta-analysis of studies revealed that many immune mediators have lower concentrations in the luteal phase compared to the follicular phase, with only a few, like IL-1α and HBD-2, showing elevated levels during luteal phase.
- The research compiled data from over 39,000 measurements, indicating a moderate to high strength of evidence for these immunological shifts throughout the menstrual cycle, highlighting a need for more comprehensive understanding due to previous inconsistent study results.
Objectives: Violence and HIV/AIDS syndemic highly prevalent among women impairs HIV prevention efforts. Prolonged exposure to violence results in physical trauma and psychological distress. Building on previous findings regarding genital immune dysregulation following sexual abuse exposure, we investigate here whether systemic changes occur as well.
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- HIV/AIDS and sexual violence negatively impact women's health, but the link between sexual violence and increased HIV vulnerability is not well understood.
- A study compared HIV-uninfected women who recently experienced sexual violence with those who hadn't, analyzing various biomarkers through blood and cervicovaginal fluid samples.
- The results showed significant immune system changes in women exposed to sexual violence, indicating that these alterations could increase their susceptibility to HIV infection.
A rise in new HIV diagnoses among older adults is characterized by poor prognosis and reduced survival times. Although heterosexual transmission remains the main route of infection in women, little is known regarding immune functions in the genital tract of postmenopausal women, especially those who are HIV positive. Furthermore, effects of hormone replacement therapy (HRT) on the genital tract immune system are unclear.
View Article and Find Full Text PDFSexual violence is associated with increased risk of HIV acquisition/transmission in women. Forced sex can result in physical trauma to the reproductive tract as well as severe psychological distress. However, immuno-biological mechanisms linking sexual violence and HIV susceptibility are incompletely understood.
View Article and Find Full Text PDFProblem: Adolescent girls are disproportionately affected by the HIV/AIDS pandemic, accounting for 22% of all new HIV infections globally. Yet little is known regarding the immune microenvironment of the adolescent female reproductive tract, especially regarding differences among sexually active and inactive girls, a critical parameter to evaluate HIV susceptibility associated with young age and sexual debut.
Methods: Cervico-vaginal lavage (CVL) was collected from sexually active (10) and inactive (8) girls aged 11-19 years and analyzed by ELISA for inflammation-associated biomarkers IL-6, IL-8, TNF-α, MIP-3α, IL-1α, IL-1β, matrix metalloproteinases (MMP) 1, 2, 7, 8, and 9, as well as anti-HIV mediators, Elafin, SLPI, human beta-defensin 2, and tissue inhibitor of matrix metalloproteinases (TIMP) 1 and 2.
Article Synopsis
- The main types of dendritic cells in skin and mucosa, Langerhans cells (LC) and interstitial dermal DC (iDDC), play crucial roles in processing antigens and activating T and B cells.
- Researchers hypothesize that these cells can be infected by human herpesvirus 8 (HHV-8), the virus associated with Kaposi's sarcoma, potentially influencing the development of this cancer.
- The study demonstrates that HHV-8 can productively infect both LC and iDDC via different receptors, impacting their ability to stimulate T cells, suggesting a significant link between HHV-8 infection and Kaposi's sarcoma pathogenesis.
Background: Rates of HIV infections are increasing in older adults. Although it is known that the HIV/AIDS epidemics affects women disproportionately, little is known regarding immune functions in the genital tract of postmenopausal women, as relevant to HIV susceptibility.
Objective: The objective of the study was to compare levels of female reproductive tract immune mediators that are important for HIV-associated immune responses as well as intrinsic anti-HIV activity in the cervical vaginal lavages collected from HIV-negative pre- and postmenopausal women.
Article Synopsis
- HIV-1-infected nonprogressors (NP) show resistance to disease progression without antiretroviral therapy due to a unique inability of their antigen-presenting cells (APC) to mediate HIV-1 trans infection of CD4(+) T cells.
- Unlike progressors (PR) and seronegative donors (SN), the APC from NP had lower cholesterol levels and higher levels of the reverse cholesterol transporter ABCA1, indicating altered lipid metabolism.
- This study suggests that the enhanced lipid metabolism in NP's APC is an inherited trait that contributes to their ability to control HIV-1 infection and prevent disease progression.
Human herpesvirus 8 (HHV-8) is the etiological agent of Kaposi's sarcoma, primary effusion lymphoma, and multicentric Castleman's disease. It is postulated that CD8(+) T cell responses play an important role in controlling HHV-8 infection and preventing development of disease. In this study, we investigated monofunctional and polyfunctional CD8(+) T cell responses to HHV-8 lytic proteins gB (glycoprotein B) and K8.
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- Human herpesvirus 8 (HHV-8) causes diseases like Kaposi's sarcoma and primary effusion lymphoma, with limited understanding of its replication in B cells despite detectable latent DNA.
- Researchers have found that activated B cells can be infected by HHV-8, leading to increased viral DNA and production of infectious virus, facilitated by the entry receptor DC-SIGN.
- The study shows that blocking DC-SIGN or endocytic pathways prevents HHV-8 infection in B cells, highlighting the importance of DC-SIGN for the virus's entry and replication in these cells.
Article Synopsis
- HIV-1 can infect T cells via a process involving dendritic cells that express DC-SIGN, which helps transfer the virus to CD4+ T cells.
- A specific group of B cells in the blood and tonsils show increased expression of DC-SIGN after stimulation, allowing them to capture and internalize HIV-1.
- The study finds that blocking DC-SIGN on B cells prevents the transmission of HIV-1 to T cells, highlighting its potential role in the progression of HIV-1 infection.
Human herpesvirus 8 (HHV-8) causes Kaposi's sarcoma and pleural effusion lymphoma. In this study, we show that dendritic cell-specific ICAM-3 grabbing nonintegrin (DC-SIGN; CD209) is a receptor for HHV-8 infection of myeloid DCs and macrophages. DC-SIGN was required for virus attachment to these cells and DC-SIGN-expressing cell lines.
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