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@#Abstract: Objective To analyze the distribution characteristics of the main pathogens of HIV/AIDS patients with wound infections and provide basis for clinical diagnosis and treatment. Methods The clinical data of 294 patients with positive secretions or pus specimens from 2016 to 2020 were analyzed retrospectively. Results A total of 357 strains of pathogenic bacteria were isolated from 294 cases, of which 123 strains of Gram-negative bacilli (G-b), accounting for 34.5%, were mainly Escherichia coli (15.4%), Klebsiella pneumoniae (3.9%), and Pseudomonas aeruginosa (3.6%); Gram-positive bacilli (G+b) 14 strains, accounting for 3.9%; 108 Gram-positive cocci (G+c), accounting for 30.3%, of which 44 strains were coagulase-positive Staphylococcus aureus (12.3%), Coagulase-negative staphylococci were mainly Staphylococcus epidermidis (4.2%) and Staphylococcus hemolyticus (2.8%); 37 strains of fungi, accounting for 10.4%, were mainly Candida albicans (5.9%); 75 strains of Mycobacterium, accounting for 21.0%, including 41 strains of Mycobacterium tuberculosis (11.5%) and 34 strains of non-tuberculosis mycobacteria (9.5%). 52 of the 294 HIV/AIDS patients had mixed infections, accounting for 17.7%. There was significant difference in the distribution of G+c, G-b, mycobacteria and mixed infection among different specimen sources (P<0.05), and there was significant difference in the distribution of mycobacteria among different CD4+T lymphocyte counts (P<0.05). There was significant difference in the level of CD4+T lymphocytes between patients of different ages (P<0.05), and there was significant difference in the level of CD4+T lymphocytes from postoperative incision and other parts (P<0.05). Conclusions Patients with HIV/AIDS are prone to combined wound infections with various pathogenic bacteria. We should strengthen the research on wound infection in HIV/AIDS patients, and timely send patients with a low number of CD4+T lymphocytes for secretion or pus culture, so as to carry out targeted treatment and improve the prognosis of patients.
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@#Abstract: Objective To investigate the distribution characteristics of HCV genotypes and subtypes in patients with HIV (human immunodeficiency virus, HIV)/HCV co-infection in Kunming based on the nucleocapsid protein gene sequence of HCV (hepatitis C virus). Methods Serum was collected from HIV/HCV co-infected patients with household registration in 14 county-level cities, districts and counties under the jurisdiction of Kunming, who admitted to Yunnan Provincial Infectious Disease Hospital from March to August 2019. The viral RNA was extracted from the serum, reverse transcribed to synthesize cDNA, and the HCV nucleocapsid protein gene-specific primers were used for nested PCR amplification. The positive amplification products were sequenced, bioinformatics software such as DNAstar and MEGAX were used for sequence analysis. Results A total of 64 samples from co-infected patients with clinical diagnosis of suspected HIV/HCV were collected and amplified by HCV nucleocapsid protein gene-specific primers, of which 17 samples were amplified positively. The results of sequence analysis showed that the sequences of 9 cases were located in the same evolutionary branch as the HCV 3b subtype sequence, and the nucleotide homology was 93.3%-95.2%; the sequences of 5 cases were located in the same evolutionary branch as the HCV 1b subtype sequence, and the nucleotide homology was 96.8%-97.6%; the sequence of one case and the subtype sequence of HCV 3a gene were located in the same evolutionary branch, and the nucleotide homology was 95.2%; the sequence of one case and HCV 6n gene subtype sequence were located in the same evolutionary branch, and the nucleotide homology was 97.9%; One case was located in the same evolutionary branch as the HCV 6u gene subtype sequence, and the nucleotide homology was 98.4%. Conclusions HCV 1b, HCV 3a, HCV 3b, HCV 6n and HCV 6u genotypes or subtypes of HCV are prevalent in Kunming, and HCV 3b is the most prevalent genotype.
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Objective@#To learn the genotypic drug resistance of men who have sex with men ( MSM ) with HIV who failed in antiviral therapy in Yunnan Province, in order to provide basis for improving the effect of antiviral therapy.@*Methods@#The patients who were infected with HIV-1, homosexual transmitted and failed in antiviral therapy in Yunnan Province from 2014 to 2019 were recruited. Their plasma samples were tested by reverse transcription nested polymerase chain reaction ( RT-nPCR ) , the fragments were spliced using ContigExpress, and the resistance to 8 protease inhibitors ( PIs ) , 7 nucleoside reverse transcriptase inhibitors ( NRTIs ) and 5 non-nucleoside reverse transcriptase inhibitors ( NNRTIs ) were obtained from the HIV drug resistance data website of Stanford University.@*Results@#A total of 205 HIV/AIDS cases were included, 169 positive plasma samples were amplified, 112 cases were drug resistant, and the rate of drug resistance was 66.27%. The patients who were aged 30-49 years ( 76.09% ) , had genotype of CRF01_AE ( 76.34% ) or treated by AZT+3TC+NVP ( 77.08% ) had higher resistance rate. The resistance rates of NNRTIs, NRTIs and PIs were 62.72%, 49.70% and 2.96%, respectively; the resistance rates of NVP and EFV in NNRTIs were 62.72% and 61.54%. The main mutation site associated with NNRTIs was K103, accounting for 21.89% ( 37 cases ) ; the main mutation site associated with NRTIs was M184, accounting for 39.64% ( 67 cases ) ; the main mutation sites associated with PIs were M46L/K, accounting for 2.96% ( 5 cases ) , resulting in high resistance to NFV.@*Conclusions@#The drug resistance rate of HIV-infected MSM with failure of antiviral therapy in Yunnan Province is relatively high, with CRF01_AE as the main gene subtype of drug resistance. The drug resistance rate of NNRTIs is relatively high, especially NVP and EFV.
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BACKGROUND: Apical periodontitis, often accompanied by periapical bone destruction, is an inflammatory disease of the periapical tissue caused by mixed bacterial infections. Studies have shown that interleukin-24 plays an important role in inflammatory response and affects bone homeostasis as a pleiotropic immune regulator. OBJECTIVE: To explore the expression of interleukin-24 during periapical periodontitis in mice. METHODS: An induced animal model was constructed in mice to simulate the progression of human apical periodontitis. Twenty-five C57BL/6 female mice at 6 weeks of age were randomly divided into five groups. Mice in the experimental group were anesthetized and the pulps of both mandibular first molars were exposed to the oral cavity for 7, 14, 21, and 28 days, named 1-, 2-, 3-, and 4-week groups. The control group was given no treatments as 0-week group. Mandibular tissues were separated in each group after anesthesia, and then were fixed, decalcified and made into frozen slices of the molar region. Hematoxylin-eosin staining was used to observe the histopathological changes of periapical lesions. Immunohistochemistry staining and RT-PCR were used to detect the expression and changes of interleukin-24 in periapical lesions of mice. The study was approved by the Animal Ethics Committee of Dalian Medical University School of Stomatology. RESULTS AND CONCLUSION: The results of hematoxylin-eosin staining showed that no obvious inflammatory response was observed in the normal periapical region of the 0-week group; the inflammatory cell infiltration area was continuously expanded and the periapical tissue was continuously destroyed in each experimental group, indicating that mouse model of periapical periodontitis was successfully established. The results of immunohistochemistry staining showed that there was almost no interleukin-24 expression in the 0-week group; the expression of interleukin-24 in the periapical region of each experimental group was significantly higher than that in the 0-week group (P < 0.05), and showed a peak expression in the 2-week group. The results of RT-PCR showed that the mRNA level of interleukin-24 in each experimental group was higher than that in the 0-week group (P < 0.05), and peaked at 2 weeks. Overall, our findings indicate that in the animal model of periapical periodontitis, the expression of interleukin-24 increases with a certain trend in the development of periapical lesions, suggesting that it may be involved in the progression of inflammation related to periapical periodontitis.