The new conception “precision medicine” has started a new era of medical practice and initiated a worldwide battle for new technologies. It essentially includes precision diagnosis and precision treatment. Its implementation in individual region may have its own uniqueness based upon the national conditions. In China, chronic infectious diseases especially tuberculosis have given rise to great burden on public health, which should be put more focus on. In fact, many modalities of precision medicine have been applied in the field of tuberculosis. Application of the concept of precision medicine throughout the study and treatment of tuberculosis will certainly contribute to the control of tuberculosis in China.

The present paper aims to investigate the clinical characterization of Talaromyces (Penicillium) marneffei cases in non-human immunodeficiency virus (HIV) patients. Nine patients diagnosed as Penicillium marneffei infection at the Department of Infectious Diseases, Huashan Hospital, Fudan University, from January 2007 to August 2017 were retrospectively enrolled. The literatures published during the same time were also reviewed. The clinical presentation, laboratory results, diagnosis and treatment were analyzed. Some patients were immunocompetent. The clinical presentations of Penicillium marneffei infection were similar in non-HIV patients and HIV patients, but most cases had a slow onset, and less fungemia. Pathology was characterized by granuloma and suppurative inflammation. Most patients were diagnosed by culture (8/9), and one patient was diagnosed by pathology and next-generation sequencing. The results suggest that Penicillium marneffei infection in non-HIV patients was increasing, and the physicians should pay more attention.

To investigate the drug resistance and virulence of Helicobacter pylori (H. pylori) strains, and explore their relationship with the infection characteristics and biofilm formation ability, gastric mucosa biopsy samples and related clinical data were collected from Huadong Hospital Affiliated to Fudan University between December 2014 and June 2015. H. pylori strains isolated from these clinical samples were subjected to drug resistance assay, virulence gene assay and biofilm-forming assay. Twenty-eight H. pylori strains were acquired. The resistance rates to levofloxacin (LEV), metronidazole (MTZ), clarithromycin (CLA) and amoxicillin (AMX) were 32%, 75%, 11% and 0, respectively. The single and double resistance rates were 61% (17/28) and 36% (10/28), respectively. The detection rates of virulence genes cagA, oipA and vacAs1 were 100%, and no vacAs2 was detected. vacAs1m2 genotype accounted for 61% (17/28), followed by vacAs1m1(11/28, 39%). The prevalence rates of iceA1, iceA2 and iceA1 iceA2 were 54% (15/28), 21% (6/28), 25% (7/28), respectively. The detection rate of dupA was 36% (10/28). The biofilm-forming ability of 28 strains varied. Single factor and independent sample t test analysis showed that strains isolated from 45-59 years old patients, iceA1^＋ dupA^－ genotype, metronidazole-sensitive strains could form stronger biofilm. In conclusion, the resistance rate of H. pylori to metronidazole was highest in single resistance, and the double resistance should not be neglected. The main genotypes of H. pylori isolates were cagA, oipA, vacAs1m2. The H. pylori biofilm-forming ability is related to the age of patients. Specifically, strains isolated from the age 45-59 group have stronger biofilm-forming ability than those obtained from other age groups. In addition, isolates carrying the virulence gene iceA1 have strong biofilm-forming ability. And there is a negative correlation between dupA genotype or metronidazole resistance and the biofilm-forming ability of the H. pylori isolates.

The present paper aimed to find out the interacting protein of hepatitis E virus (HEV) capsid protein ORF2 and explore its role in HEV infection. CD63 was identified as a potential HEV ORF2-interacting protein by screening a human liver cDNA library for yeast two-hybrid method. Co-immunoprecipitation and pull-down assays were used to verify the interaction. The expression of cell surface CD63 was detected by flow cytometry in HEV susceptible, non-susceptible and overexpressed cells (PLC/PRF/5) respectively. HEV infectivity was measured through virus infection assay. The results indicated that expression level of CD63 on the cell membrane of HEV susceptible cell lines was lower than that of HEV non-susceptible cell lines. Overexpression of CD63 inhibited the HEV infection of PLC/PRF/5 cells, while siRNA interference of CD63 promoted the HEV infection. The results indicated that CD63 could interact with HEV ORF2, and may inhibit HEV infection in hepatocytes.

Experimental course is an essential and indispensable part of modern medical microbiology teaching. Unfortunately, in the reform of experiment teaching of medical microbiology, we often overlook the importance of the preparation of experimental course in fulfilling high-quality teaching. In this paper, we reviewed the status of medical microbiological experimental course in three stages: before 2000, 2000-2010 and 2011-present. Then we analyzed and discussed on the considerations in the preparation of experimental courses as well as the requirements of experimental conditions, and suggested that highly competent technicians play an important role in experiment teaching of medical microbiology.

The increasing rate of drug resistance in tuberculosis possesses a great challenge to the global tuberculosis control. The drug resistance in Mycobacterium tuberculosis (M. tuberculosis) is mainly conferred by chromosomal mutations in essential and highly conserved genes, and usually accompanied by a reduction in fitness, namely “fitness cost”. However, this fitness cost can be ameliorated by secondary compensatory mutations which help restore the fitness of drug-resistant strains. The compensatory evolution has been regarded as the biological basis of the extensive spread and high prevalence of drug-resistant M. tuberculosis. Recently, a series of scientific works in the field of molecular epidemiology of tuberculosis and the basic research on the compensatory evolution of drug-resistant M. tuberculosis have been conducted. In this review, we focus on the molecular mechanisms for fitness cost of drug resistance, the compensatory evolution and the potential impacts of these two processes on the transmission of M. tuberculosis.

In recent years, the emergence of multidrug-resistant tuberculosis (MDR-TB) and the increase of co-infection of human immunodeficiency virus (HIV) and tuberculosis have led to more severe challenges in the prevention and treatment of tuberculosis. It is urgent to develop new anti-tuberculosis drugs and natural adjuvant therapy with low toxicity. The catechins in green tea have a variety of biological activities, and have shown a certain adjuvant therapeutic effect on many diseases. Studies have shown that catechins also have anti-tuberculosis activities, and the mechanisms include inhibition of dihydrofolate reductase, affecting mycolic acid and cell wall synthesis, down-regulation of tryptophan-aspartate containing coat protein (TACO) gene expression to inhibit the growth of intracellular Mycobacterium tuberculosis, reducing oxidative stress, down-regulation of Mycobacterium tuberculosis 85B and tumor necrosis factor α (TNF-α) levels to alleviate the inflammation. It is also proved that drinking green tea can reduce the susceptibility to tuberculosis, and catechins can be an adjuvant therapy of tuberculosis and have a synergistic effect with anti-tuberculosis drugs. However, the anti-tuberculosis mechanisms of catechins are unclear, and more trials are needed to confirm the anti-tuberculosis activity of catechins.

Mycobacterium tuberculosis (M. tuberculosis) is causative pathogen of tuberculosis, and could induce long-term asymptomatic infection, known as latent tuberculosis infection (LTBI), in which the bacteria are thought to persist in a dormant state. It is reported that there are pairs of toxin-antitoxin systems (TASs) in chromosomes of M. tuberculosis. Some TASs play roles in the latent infection because they could not only regulate the bacterial growth, but also induce the bacteria to enter dormant state. Some TASs are suggested to be involved in the biofilm formation and stress reaction, but how they regulate biofilm formation has not yet been elucidated. M. tuberculosis in biofilm is resistant to many drugs and host immune protections. M. tuberculosis in dormant state is usually multidrug-resistant. These issues bring challenges for the treatment of tuberculosis. This review focuses on the research progress on TAS and biofilm formation of M. tuberculosis, as well as the effect of anti-tuberculosis drugs on biofilm formation.

Detection rate of Candida tropicalis (C. tropicalis) is increasing in clinical practice. Azole antifungal agents are commonly used in the treatment of C. tropicalis infection because of their low cytotoxicity and oral administration. In China, there is a high rate of isolation of azole resistant C. tropicalis. It is necessary to understand the azole resistance mechanism of C. tropicalis, which may provide a base for new drug targets. At present, the main mechanisms associated with resistance of C. tropicalis to azoles are the overexpression and mutation of the target gene ERG11, the overexpression and mutation of upc2 gene encoding a transcription factor, the overexpression of efflux pump genes and other related genes. In this paper, the current progress on the latest azole resistance mechanism of C. tropicalis is reviewed.

As a member of bicomponent pore-forming leucocidins from Staphylococcus aureus (S. aureus), leukocidin ED (LukED) is encoded by two linked genes (lukE and lukD), which are co-transcribed into one mRNA. LukED is found to be able to target the chemokine receptor CCR5 to kill inflammatory macrophages, T cells, and dendritic cells, or to target receptor CXCR1/2 on neutrophils, monocytes and natural killer (NK) cells to enhance pathogenicity of S. aureus and death of the host. In addition, LukED can also lyse erythrocytes to release hemoglobin by binding to the Duffy antigen receptor for chemokines, and further promote the absorption of iron and growth of bacteria. The expression of LukED is regulated by the accessory gene regulatory-repressor of toxins (agr-rot) pathway and transcriptional regulators such as RpiRc and SpoVG. Studies show that lukED genes have a high frequency in S. aureus and have a close association with bloodstream infection, impetigo and antibiotic-associated diarrhea. Progress on researches of LukED not only improves our knowledge about clinical importance and the pathogenesis of S. aureus, but also provides insight into the development of potential novel anti-toxin drugs for the treatment of S. aureus infection.