Association between cervical shedding of herpes simplex virus and HIV-1
ABSTRACT To investigate the association between the cervical shedding of herpes simplex virus (HSV) and HIV-1.
A cross-sectional study on 200 women seropositive for both HSV-2 and HIV-1 was conducted in a family planning clinic at the Coast Provincial General Hospital, Mombasa, Kenya.
Quantities of HSV DNA (types 1 and 2) and HIV-1 RNA as well as the presence or absence of HIV-1 proviral DNA in cervical secretions were determined and compared.
There was a significant correlation between the quantities of HSV DNA and HIV-1 RNA in the cervical secretions of HSV-shedding women (Pearson's r = 0.24, P = 0.05). A 10-fold increase in the quantity of cervical HSV DNA was associated with 1.35-fold higher cervical HIV-1-RNA levels (95% CI 1.00-1.81; P = 0.05), and with 1.36-fold greater odds of detection of HIV-1 proviral DNA (95% CI 1.05-1.75; P = 0.02).
Higher levels of cervical HSV were associated with higher levels of expressed HIV-1 and with the more frequent detection of HIV-1-infected cells in cervical secretions. Prospective studies are needed to explore further the association between non-ulcerative cervical HSV reactivation and HIV-1 shedding. Such a relationship may have important implications for interventions designed to slow the spread of HIV-1.
- SourceAvailable from: Dimitra Kovala-Demertzi
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- "Herpes simplex viruses (HSVs) are highly adapted human pathogens with rapid lytic cycle and ability to invade sensory neurons.The primary agents of recurrent facial and genital herpes lesions are HSV-1 and HSV-2 while genital herpes (GH) is the most common sexually transmitted infection in the world   . Moreover, GH is the main factor of increasing three to five times the risk of HIV transmission, stimulating HIV replication, and finally leading to the progression of AIDS   . Acyclovir (ACV) is a prodrug and it is the first nucleoside-based therapeutic effective for the treatment D. Kovala-Demertzi, P. Genova, P. Souza, and M. A. Demertzis dedicate this work to the late Professor T. Varadinova for her contribution to virology. "
ABSTRACT: The cytotoxicity and the antivirus activity of Pd(II) and Pt(II) complexes with pyridine-2-carbaldehyde thiosemicarbazone (HFoTsc) against HSV replication were evaluated on four HSV strains—two wt strains Victoria (HSV-1) and BJA (HSV-2) and two ACVR mutants with different tk gene mutations R-100 (TKA, HSV-1) and PU (TKN, HSV-2). The experiments were performed on continuous MDBK cells and four HSV 1 and HSV 2 strains were used, two sensitive to acyclovir and two resistant mutants. The five complexes of HFoTsc, [Pt(FoTsc)Cl], [Pt(FoTsc)(H2FoTsc)]Cl2, [Pt(FoTsc)2], [Pd(FoTsc)(H2FoTsc)]Cl2, and [Pd(FoTsc)2], were found to be effective inhibitors of HSV replication. The most promising, active, and selective anti-HSV agent was found to be complex [Pt(FoTsc)(H2FoTsc)]Cl2. This complex could be useful in the treatment of HSV infections, since it is resistant to ACV mutants. PCR study of immediate early 300 bp ReIV Us1 region reveals that the complex [Pt(FoTsc)(H2FoTsc)]Cl2 specifically suppressed wt HSV-1 genome 2 hours after the infection, not inducing apoptosis/necrosis on the 8 hours after virus infection. The target was found to be most probably the viral, instead of the host cell DNA.Bioinorganic Chemistry and Applications 02/2007; 2007:56165. DOI:10.1155/2007/56165 · 1.66 Impact Factor
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- "HSV promotes HIV replication in human T cells (Mosca et al., 1987) and in macrophages by inducing NF-κB activity (Moriuchi et al., 2000). Increased HIV viral shedding can also be found in subclinical non-ulcerative HSV (Mbopi Keou et al., 1999; McClelland et al., 2002) suggesting that HIV transmissibility may be enhanced without direct mucosal disruption and herpetic ulceration. Ongoing clinical trials are evaluating the role of acyclovir in reducing HIV transmission. "
ABSTRACT: Antecedent or current infections can alter the immunopathologic outcome of a subsequent unrelated infection. Immunomodulation by co-infecting pathogens has been referred to as 'heterologous immunity' and has been postulated to play a role in host susceptibility to disease, tolerance to organ transplant, and autoimmune disease. The effect of various infections on heterologous immune responses has been well studied in the context of shared epitopes and cross-reactive T cells. It has been shown that prior infections can modulate protective immunity and immunopathology by forming a pool of memory T cells that can cross-react with antigens from heterologous organisms or through the generation of a network of regulatory cells and cytokines. While it is not feasible to alter a host's history of prior infection, understanding heterologous immune responses in the context of simultaneous unrelated infections could have important therapeutic implications. Here, we outline key evidence from animal and human studies demonstrating the effect of heterologous immunity on the outcome of disease. We briefly review the role of T cells, but expand our discussion to explore other immune mechanisms that may modulate the response to concurrent active infections. In particular, we underscore the role of the innate immune system, polarized responses and regulatory mechanisms on heterologous immune responses.Cellular Microbiology 03/2006; 8(2):185-96. DOI:10.1111/j.1462-5822.2005.00653.x · 4.82 Impact Factor