Influence of Staphylococcus aureus attachment to the herpes simplex virus infected cells.

The purpose of this study was to investigate the response of HeLa cells to the interaction with inactivated Staphylococcus aureus cells and live challenge with herpes simplex virus (HSV).The results of this study are indicating that the interaction between the HeLa cells and S. aureus inactivated whole cells could modulate the host cell apoptosis and cytokine production, and therefore, influence the progression of HSV infection. The pre-treatment of HeLa cells with heat inactivated bacterial whole cells protects them from the occurrence of HSV mediated cytopathic effect, while the post viral infection treatment with bacterial cells prevents the high activation of bax/bcl-2 apoptotic pathway, a process that could change the fate of the infectious process triggered by the virus, and eventually reduce its multiplication rate. The pre-treatment of HeLa monolayer with inactivated bacterial cells 24 hours before the viral infection is increasing the expression level of TNF-a, IL-6 and IL-8 pro-inflammatory cytokines genes, also suggesting that bacterial antigens could contribute to the decrease of viral multiplication rate.

MECHANISMS OF THROMBOSIS IN SYSTEMIC LUPUS ERYTHEMATOSUS.

Thrombotic events are highly prevalent in systemic lupus erythematosus (SLE). Antiphospholipid antibodies play an essential role in promoting thrombosis by activating several intracellular signaling pathways (TLR4, p38MAPK, NFkB) in platelets, monocytes and endothelial cells. New therapeutic opportunities might be offered by addressing these molecular targets. Chronic inflammatory status, the degree of disease activity and accelerated atherosclerosis are also responsible for the thrombotic phenotype in patients with SLE. The aim of this review is to highlight thrombosis mechanisms and to look for possible connection between SLE, antiphospholipid antibodies and cancer, especially myeloproliferative neoplasms.

Tracking down of laryngo-pharyngeal metastasis.

BACKGROUND: In Romania, the most optimistic statistics give a 5 years survival rate in approximately 33% of laryngo-pharyngeal cancer patients. Considering that a cell carrying the viral DNA is originating from primary tumor, we have tested whether HPV DNA could be detected in the blood cell of patients with laryngeal cancer as a marker of disease progression and metastases. METHODS: The study was performed on 85 patients (59 +/- 8.7 age) with laryngo-pharyngeal cancer. HPV DNA was detected in tumor using nested PCR with consensus primers, and also in local lymph nodes and/or blood cells from patients HPV positive in primary tumor. RESULTS: HPV DNA was detected in 75.29% of analyzed tumours, and all HPV16 positive samples were confirmed by mRNA E6 expression. 56.3% of patients presented HPV DNA in peripheral circulation as confirmed by PCR with E6 HPV16 specific primers followed by Southern Blot. CONCLUSION: Our results sustain that the detection of HPV DNA in blood is a "surrogate marker" of metastasis when extension of metastasis cannot be estimated, this observation is very important for management of cancer patients with laryngopharyngeal localization.