Infectious

Figure 1. Laboratory facility infrastructure and accreditation overview. The top section illustrates the government accreditation process alongside key operational areas, including biosafety workspaces, cleanrooms, animal housing, and sterilization units. The bottom section outlines the specific list of pathogens managed at the facility.

                                                                                  The IC50 of ACV with HSV-1 in vitro cell line                                                                 The IC50 of Ziresovir with RSV infection in Hep2 cells

                                                                                                   Plaque assays with HSV-2 virus                                                                   CPE observation of H1N1 in MDCK cells

                                                        Viral load in vaginal tissue in HSV-2 infection model                       Neutralizing Serum Hemagglutination Inhibition Assay for influenza vaccine

Figure 2. In vitro and in vivo virological assays for viral quantification and antiviral efficacy evaluation.

Virus infection models in mice are used to study the pathogenesis of viral diseases and evaluate the efficacy of antiviral drugs in a living organism. By infecting mice with specific viruses, we can observe how the virus spreads, replicates, and causes disease symptoms. This allows us to test the ability of experimental drugs to reduce viral load, improve survival rates, and alleviate disease symptoms in a more physiological context.

Table 1.Model and drug evaluation corresponding to different viruses.

The study outline of  influenza vaccine validation

The bodyweight, survival rate, histological changes and viral load examination in H1N1 vaccine validation project

Figure 3: Experimental design and in vivo efficacy evaluation of vaccine candidates against Influenza A Virus (IAV). The data is expressed as mean ±SEM.

Figure 4: The AAV-HBV transduction model enables efficient delivery of multiple HBV genotypes into target cells, closely mimicking the natural infection process. This model supports the study of HBV replication and pathogenesis, as well as the preclinical evaluation of antiviral therapeutics and vaccine candidates.

Figure 5.Generation of human liver chimeric mice and evaluation of in vivo Hepatitis B Virus (HBV) infection.

(a) Serum human albumin levels (mg/ml) at week 8 and week 15, confirming the successful and stable engraftment of primary human hepatocytes (PHHs).(b) Representative immunohistochemistry (IHC) images of liver sections from uninfected hu-NCG-FAH-KO mice (left) and HBV-infected hu-NCG-FAH-KO mice (right).(c) Dynamic monitoring of serum HBV virological markers at weeks 8, 12, and 15 post-infection:  Serum HBsAg levels (IU/ml);  Serum HBeAg levels (NCU/ml); Serum HBV DNA loads (log10 copies/ml).The data is expressed as mean±SEM.

MIC is the lowest concentration of an antibacterial agent that inhibits the visible growth of bacteria. We use methods such as broth dilution, agar dilution, and E-test to accurately determine the MIC of various antibacterial drugs against different bacterial strains.

MBC is the lowest concentration of an antibacterial agent that kills bacteria. After determining the MIC, we further conduct experiments to find the MBC. 

Bacteria and fungus culture

Bacterial infection models involve infecting mice with pathogenic bacteria to study the host-pathogen interaction and evaluate the efficacy of antibacterial drugs. We can use different routes of infection, such as intravenous, intraperitoneal, or subcutaneous injection, to mimic different types of human infections. This helps in assessing the in vivo efficacy of drugs in treating bacterial infections and understanding the development of resistance.

Table 1.Model and drug evaluation corresponding to different bacteria and fungus.

Figure 6. Establishment and evaluation of a Staph. aureus ABSSSI model. Schematic representation of the study design. Subjects were subcutaneously injected at Day 0 with either PBS (G1, control) or varying doses of SA: low (G2), medium (G3), and high (G4).(a) Body weight changes. Daily monitoring of body weights across all groups over the 7-day post-infection period.(b) Area of skin abscess. Kinetic quantification of macroscopic skin abscess progression over the 7-day observation period, demonstrating a dose-dependent increase in lesion size.(c) Skin wound score. Clinical evaluation of skin wound severity at day 7 post-infection.(d) and (e) Histopathological evaluation. Representative Hematoxylin and Eosin (H&E) stained skin tissue sections from all experimental groups on day 7. Gross macroscopic images of the lesions are shown in the bottom-left insets of the main overview panels. The data is expressed as mean±SEM.

Figure 7. Experimental outline and in vivo evaluation of the P. aeruginosa infection model. Schematic representation of the study design and timeline.  Daily body weight changes of the subjects over the 7-day observation period following bacterial administration.  Representative H&E-stained sections of lung tissues collected at termination, illustrating varying degrees of pulmonary inflammation, cellular infiltration, and histological alterations across the experimental groups. The data is expressed as mean±SEM.

Figure 8. Experimental design and evaluation of a respiratory co-infection model. Schematic overview of the study timeline, involving H1N1 viral infection followed by secondary infection (Aspergillus / PA), detailing periods for monitoring body weight and survival, leading up to study termination for histology and cytokine analysis. Time-course evaluation of body weight changes across the experimental groups over the observation period. Representative H&E-stained lung histology sections from the different cohorts (G1: NC+PA-1E6, G2: H1N1+PA-1E6, G3: H1N1+PA-1E7, and H1N1 only). The panels illustrate varying severities of pulmonary inflammation, cellular infiltration, and structural damage to the lung tissue. Quantification of the inflammatory cytokine IL-1β in lung tissue homogenates and bronchoalveolar lavage fluid (BALF) across the groups. The data is expressed as mean±SEM. *p < 0.05; **p < 0.01; ***p < 0.001.

Fungal sepsis caused by Candida albicans in immunocompetent mice

Figure 9. Establishment and evaluation of a systemic Candida infection model. Schematic overview of the experimental design, depicting intraperitoneal (i.p.) administration of Candida, monitoring parameters, and endpoint tissue collection. Daily body weight monitoring of C57BL/6JGpt mice administered with PBS (G1) or varying concentrations of Candida (G2-G5) over a 7-day period. Kaplan-Meier survival curves for the respective experimental groups post-infection.  Quantification of fungal burden (CFU/mL) across different organs (lung, liver, spleen, and kidney) in the G2 and G3 cohorts. Representative H&E-stained histological sections of the lung, liver, and kidney from the PBS control (G1), G2, and G3 groups. The data is expressed as mean±SEM.