Human immunodeficiency virus (HIV) is one of the critical infectious agents with thousands of newly infected people worldwide. High mutational capability and rapid diversification, inhibition of humoral and cellular immune responses, and thus inability for recognition of an immunogenic region in the viral envelope by the immune system are major challenges. Natural killer (NK) cells are multifunctional, playing a key role in the identification and elimination of HIV‐infected cells. These cells identify and eliminate virus‐infected cells in a multilateral manner, such as ligand stress, antibody‐dependent cell cytotoxicity (ADCC), T follicular helper (Tfh), and the activation of most of the stimulatory receptors. Moreover, these cells release cytokines leading to the activation of cytotoxic lymphocytes (CTLs) and dendritic cells (DCs), contributing to efficient viral elimination. Some subsets of NK cells exhibit putatively enhanced effector functions against viruses following vaccination easily expanded and identified by NK cell lines culture. Furthermore, NK cells promote the elimination of HIV‐infected cells which reduce the expression of major histocompatibility complex (MHC) molecules. Memory NK cells have higher functionality and renewable potential. A pioneering strategy to establish an efficacious HIV vaccine would include stimulation of the accumulation and long‐term maintenance of these HIV‐reactive NK cells. CAR‐NK (chimeric antigen receptor‐natural killer) cells‐based antiviral therapies have emerged as novel approaches with the ability of antigen recognition and more advantages than CAR‐T (chimeric antigen receptor‐T) cells. Recent development of induced pluripotent stem cell (iPSC)‐derived NK cells with enhanced activity and efficiency conferred a promising insight into CAR‐NK cell‐based therapies. Therefore, memory and CAR‐NK cells‐based approaches can emerge as novel strategies providing implications for HIV vaccine design and therapy.
Introduction:Pseudomonas aeruginosa isolates are among the most common pathogens causing nosocomial infections. They are intrinsically resistant to most of antibiotics such as novel β-lactams and therefore, can develop resistance during treatment, culminating in failure in remedy. Objectives: The aim of this study was to detect the genes encoding class A extended-spectrum betalactamases (ESBLs) such as PER-1, VEB-1 and PSE-1 among P. aeruginosa isolates from intensive care unit (ICU) patients. Materials and Methods: A total of 65 isolates were collected from ICU in three hospitals of Tehran in 2016. The antibiotic susceptibility test was conducted according to Clinical and Laboratory Standards Institute (CLSI) guideline. MIC of ceftazidime was done with agar dilution method. The combine disk test was performed for detection of isolates producing ESBLs. Polymerase chain reaction (PCR) was performed to detect the PER-1, VEB-1 and PSE-1 genes using specific primers. Results: Fifty-four percent (n=38) of patients were male and 46% (n=27) were female. The majority of ICU isolates were resistant to augmentin (93.8%, n=61) and cefpodoxime (84.8%, n=56). Fifty (77%) isolates were ESBL positive, among which 94% (n=47) harbored PER-1 gene followed by 52% (n=26) VEB-1 and 16% (n=8) PSE-1 genes. Conclusion: Concomitance presence of bla PER1 and bla VEB1 was observed among 10 isolates, and 7 amplified all these three genes. A high number of ICU P. aeruginosa isolates were ESBL producers. The frequency of bla VEB1 and bla PER1 were relatively high, while bla PSE1 was detected among a low number of isolates. Moreover, resistance to carbapenems was low. It is necessary to follow up ICU centers because of drugresistant P. aeruginosa isolates. AbstractCitation: Ghasemian A, Shokouhi Mostafavi SK, Eslami M, Vafaei M, Nojoomi F, Hasanvand F. Antibiotic resistance and presence of bla PER-1 , bla VEB-1 and bla PSE-1 beta-lacamases among clinical isolates of Pseudomonas aeruginosa from ICU settings. Immunopathol Persa. 2018;4(2):e26.
Background and objective: Among the Candida species, Candida glabrata (C. glabrata) is inherently resistant to anti-mycotic agent, azole. The aim of this study was to assess the effects of Aspirin as an anti-inflammatory drug on azole-resistant Candida glabrata in-vitro.
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