Effect of 48-week pegylated interferon α-2a or nucleos(t)ide analogue therapy on renal function in Chinese patients with chronic hepatitis B.

BACKGROUND: Controversy remains as to whether antiviral agents contribute to renal dysfunction in patients with chronic hepatitis B virus (HBV) infection. Thus, the aim of study was to analyze the changes in renal function of chronic hepatitis B (CHB) patients in response to anti-HBV therapy and the association with treatments. METHOD: We performed a retrospective observational cohort study to investigate factors associated with renal function in 249 Chinese CHB patients who were treated with pegylated interferon α-2a (PEG-IFN-α-2a) or nucleos(t)ide analogues for 48 weeks. Changes of estimated glomerular filtration rate (eGFR), which was computed with both the Chronic Kidney Disease Epidemiology Collaboration and the Modification of Diet in Renal Disease formulas, were tested by repeated measures One-way analysis of variance within groups. A linear mixed effects model for repeated measures was also used to evaluate the association between baseline information and eGFR changes over time in all enrolled patients. The model considered the baseline age, sex, HBV DNA, aminotransferase, blood urea nitrogen, treatment group, time, and group-by-time interaction as fixed effects and incorporated random effects for individual subjects. RESULTS: The eGFR increased in patients given PEG-IFN-α-2a, decreased in patients given adefovir, but remained stable in patients given entecavir. Age and blood urea nitrogen were significant negative predictive factors for eGFR changes. CONCLUSION: In real-life study, PEG-IFN-α-2a therapy in CHB patients increased eGFR, thus may associate with renoprotective effects when compared with adefovir or entecavir therapies.

Humanized-BLT mouse model of Kaposi's sarcoma-associated herpesvirus infection.

Lack of an effective small-animal model to study the Kaposi's sarcoma-associated herpesvirus (KSHV) infection in vivo has hampered studies on the pathogenesis and transmission of KSHV. The objective of our study was to determine whether the humanized BLT (bone marrow, liver, and thymus) mouse (hu-BLT) model generated from NOD/SCID/IL2rγ mice can be a useful model for studying KSHV infection. We have tested KSHV infection of hu-BLT mice via various routes of infection, including oral and intravaginal routes, to mimic natural routes of transmission, with recombinant KSHV over a 1- or 3-mo period. Infection was determined by measuring viral DNA, latent and lytic viral transcripts and antigens in various tissues by PCR, in situ hybridization, and immunohistochemical staining. KSHV DNA, as well as both latent and lytic viral transcripts and proteins, were detected in various tissues, via various routes of infection. Using double-labeled immune-fluorescence confocal microscopy, we found that KSHV can establish infection in human B cells and macrophages. Our results demonstrate that KSHV can establish a robust infection in the hu-BLT mice, via different routes of infection, including the oral mucosa which is the most common natural route of infection. This hu-BLT mouse not only will be a useful model for studying the pathogenesis of KSHV in vivo but can potentially be used to study the routes and spread of viral infection in the infected host.

Imbalance of regulatory T cells and T helper type 17 cells in patients with chronic hepatitis C.

Pegylated interferon and ribavirin combination therapy is known to be effective in suppressing viral replication in 50-60% of hepatitis C virus (HCV)-infected patients. However, HCV-infected patients often exhibit varied responses to therapy. Therefore, the identification of immunological markers associated with the clinical outcomes of antiviral treatment is critical for improvement of therapeutic options. In this study, we aimed to investigate the ratio of CD4(+) CD25(+) FoxP3(+) regulatory T (Treg) cells to interleukin-17A (IL-17A) -producing T helper type 17 (Th17) cells, and its association with clinical outcomes in response to anti-HCV treatment. In all, 114 patients with HCV infection received pegylated interferon-α2a and ribavirin therapy for 48 weeks, and the frequency of Treg cells and Th17 cells as well as the levels of secreted cytokines were longitudinally analysed by flow cytometry and ELISA. Treg cell proportions and IL-10 production were significantly elevated in HCV-infected patients, especially for HCV genotype 1b. However, the frequency of Th17 cells as well as the secretion of IL-17, IL-22 and IL-23 did not reveal notable difference between HCV infections and healthy individuals. Inhibition of HCV replication was accompanied by a reduction in Treg cells, but little influence on Th17 cells, which led to a significant decrease in Treg : Th17 ratios. Skewed Treg : Th17 ratios existed in chronic hepatitis C. HCV RNA load is closely associated with Treg : Th17 ratios during pegylated interferon-α2a and ribavirin treatment in HCV-infected patients. The imbalance of Treg cells to Th17 cells might play an important role in persistent HCV infection.

[Research progress on the relationship between low-density neutrophils and infectious diseases].

Neutrophils play an important role in infectious diseases by clearing pathogens in the early stages of the disease and damaging the surrounding tissues along with the disease progress. Low-density neutrophils (LDNs) are a crucial and distinct subpopulation of neutrophils. They are a mixture of activated and degranulated normal mature neutrophils and a considerable number of immature neutrophils prematurely released from the bone marrow. Additionally, they may be involved in the occurrence and development of diseases through the changes in phagocytosis, the generation of reactive oxygen species (ROS), the enhancement of the ability to produce neutrophils extracellular traps and immunosuppression. We summarizes the role of LDNs in the pathogenesis and their correlation with the severity of infectious diseases such as COVID-19, severe fever with thrombocytopenia syndrome (SFTS), AIDS, and tuberculosis.

An improved sulfur-nitroso-proteome strategy for global profiling of sulfur-nitrosylated proteins and sulfur-nitrosylation sites in mice.

Comprehensive sulfur-nitrosylation (SNO) proteome coverage in complex biological systems remains challenging as a result of the low level of endogenous S-nitrosylation and its chemical instability. Herein, we optimized the synthesis route of SNOTRAP (SNO trapping by triaryl phosphine) probe and the proteomics pipeline (including preventing over-alkylation, sample washing, trypsin digestion). Preventing overalkylation was found to be the key factor resulting in a higher number of identified SNO proteins by evaluating various experimental conditions. With the improved SNOTRAP-based proteomic pipeline, we achieved an improvement of ∼10-fold on identification efficiency, and identified 1181 SNO proteins (1714 SNO sites) in mouse brain, representing the largest repository of endogenous S-nitrosylation. Moreover, we identified the consensus motif of SNO sites, suggesting the correlation with local hydrophobicity, acid-base catalysis, and the surrounding secondary structures for modification of specific cysteines by NO. Collectively, we provide a universal pipeline for the high-coverage identification of low-abundance SNO proteins with high enrichment efficiency, high specificity (98%), good reproducibility, and easy implementation, contributing to the elucidation of the mechanism(s) of nitrosative stress in multiple diseases.

Impact of inactivated vaccines on decrease of viral RNA levels in individuals with the SARS-CoV-2 Omicron (BA.2) variant: A retrospective cohort study in Shanghai, China.

Background: SARS-CoV-2 Omicron (BA.2) has stronger infectivity and more vaccine breakthrough capability than previous variants. Few studies have examined the impact of inactivated vaccines on the decrease of viral RNA levels in individuals with the Omicron variant, based on individuals' continuous daily cycle threshold (Ct) values and associated medical information from the infection to hospital discharge on a large population. Methods: We extracted 39,811 individuals from 174,371 Omicron-infected individuals according to data inclusion and exclusion criteria. We performed the survival data analysis and Generalized Estimating Equation to calculate the adjusted relative risk (aRR) to assess the effect of inactivated vaccines on the decrease of viral RNA levels. Results: Negative conversion was achieved in 54.7 and 94.3% of all infected individuals after one and 2 weeks, respectively. aRRs were shown weak effects on turning negative associated with vaccinations in asymptomatic infections and a little effect in mild diseases. Vaccinations had a protective effect on persistent positivity over 2 and 3 weeks. aRRs, attributed to full and booster vaccinations, were both around 0.7 and had no statistical significance in asymptomatic infections, but were both around 0.6 with statistical significance in mild diseases, respectively. Trends of viral RNA levels among vaccination groups were not significant in asymptomatic infections, but were significant between unvaccinated group and three vaccination groups in mild diseases. Conclusion: Inactivated vaccines accelerate the decrease of viral RNA levels in asymptomatic and mild Omicron-infected individuals. Vaccinated individuals have lower viral RNA levels, faster negative conversion, and fewer persisting positive proportions than unvaccinated individuals. The effects are more evident and significant in mild diseases than in asymptomatic infections.

Design, synthesis, and tumor drug resistance reversal activity of novel hederagenin derivatives modified by nitrogen-containing heterocycles.

The emergence of multidrug resistance (MDR) in tumors leads to reduced chemotherapeutic efficacy, and P-glycoprotein (P-gp) overexpression is one of the main causes of MDR. In previous reports, we demonstrated that a variety of hederagenin (HD) derivatives could reverse MDR in tumors in vivo and in vitro. To further enrich the structure types, enhance the activity, and improve the structure-activity relationships (SARs), three series of HD derivatives were designed and synthesized in this study via A-ring fusion and innovative utilization of the structural advantages of nitrogen-containing heterocycles and benzyl group substitution. We evaluated the MDR reversal activity of 21 HD derivatives in KBV (multidrug-resistant oral epidermoid carcinoma) cells and refined their SARs. The results of cell experiments illustrated that more than half of the compounds had MDR reversal activity. Among them, compound 16 displayed relatively stronger MDR reversal ability, as it improved the sensitivity of KBV cells to paclitaxel, vincristine, mitoxantrone and cisplatin with IC50 values of 3.19, 0.65, 125.30, and 4.54 nM, respectively. The results of mechanistic analysis demonstrated that compound 16 inhibited the efflux function of P-gp by activating P-gp ATPase and increased the accumulation of rhodamine 123 in KBV cells. Importantly, the efficacy of paclitaxel against KBV cancer cell-derived xenograft tumors in nude mice was enhanced by compound 16 based on the growth suppression rate of 56.24%. These results indicated that introducing nitrogen-containing heterocycles could effectively improve the MDR reversal activity of HD derivatives, which appear to be promising lead compounds for tumor MDR reversal agent development.

Anti-Colorectal Cancer Effects of a Novel Camptothecin Derivative PCC0208037 In Vitro and In Vivo.

Colorectal cancer is one of the most common malignancies, and the topoisomerase inhibitor irinotecan (CPT-11)-based chemotherapeutic regimen is currently the first-line treatment with impressive therapeutic efficacy. However, irinotecan has several clinically significant side effects, including diarrhea, which limit its clinical utility and efficacy in many patients. In an effort to discover better and improved pharmacotherapy against colorectal cancer, we synthesized a novel topoisomerase inhibitor, PCC0208037, examined its anti-tumor efficacy and related molecular mechanisms, and characterized its toxicity and pharmacokinetic profiles. PCC0208037 suppressed colorectal cancer cell (CRC) proliferation and increased cell cycle arrest, which may be related to its effects on up-regulating DNA damage response (DDR)-related molecules and apoptosis-related proteins. PCC0208037 demonstrated robust anti-tumor activity in vivo in a colorectal cancer cell xenograft model, which was comparable to or slightly better than CPT-11. In a preliminary toxicology study, PCC0208037 demonstrated much weaker tissue damage to colorectal tissue than CPT-11, and its impacts on food intake and body weight loss were more transient and recovered faster than CPT-11 in mice. This could be partially explained by the pharmacokinetic findings, which showed that PCC0208037 and its active metabolite, SN-38, were more accumulated in tumor tissue than in the intestine, as compared to CPT-11. Taken together, these results described a novel Topo I inhibitor with a comparative advantage over the standard treatment of colorectal cancer CPT-11 and could be a promising candidate compound for the treatment of colorectal cancer that warrants further investigation.

A human immunodeficiency virus-seronegative acquired immunodeficiency syndrome patient with opportunistic infections: A case report.

BACKGROUND: In rare cases, people living with chronic human immunodeficiency virus (HIV) infection do not develop antibodies despite demonstrable infection. Delayed or missed diagnosis of HIV infection leads to a lack of timely therapy, resulting in rapid disease progression with opportunistic infections or malignancies. CASE REPORT: A 44-year-old Chinese man presented with sore throat, oral leukoplakia, fever, dyspnoea and diffuse ground glass-like lesions in both lungs. Serum cytomegalovirus DNA was detectable, and CD4+ T-cell count was low. The patient was suspected of being a person living with HIV despite of the repeatedly negative HIV antibody tests using enzyme-linked immunsorbent assay and Western blot. Subsequently, high-plasma HIV RNA viral load was found on two repeated tests, while HIV DNA was also positive. Thus, the patient was confirmed as presenting with HIV-seronegative acquired immunodeficiency syndrome (AIDS). The symptoms improved in response to effective anti-fungal and anti-retroviral therapy after diagnosis. CONCLUSION: This is the third reported case of an HIV-seronegative AIDS patient in China, which are also rarely reported globally. HIV nucleic acid testing is important to screen out HIV infection, especially in those who present with severe immunodeficiency but remain HIV serogenative.

Study on clinical characteristics of 173 cases of COVID-19 and effect of glucocorticoid on nucleic acid negative conversion.

Objective: To study the clinical characteristics, changes in relevant test parameters, time of nucleic acid negative conversion, and effect of glucocorticoid treatment in Wuhan area patients with the novel coronavirus pneumonia (COVID-19). Methods: Data of 173 inpatients at Huoshenshan Hospital from February 10 to March 17, 2020, were analyzed retrospectively. Clinical characteristics, partial test results, and the influence of glucocorticoid therapy on the clinical outcomes of nucleic acid negative conversion and changes in lung CT images were compared. The patients were divided at admission into 4 groups according to the course of disease and glucocorticoid treatment. Differences among the groups were analyzed statistically. Results: The median age of 173 patients was 62 years, and 91.3% were over 40 years old. Underlying diseases occurred in 50.3% of patients, 32.6% had family gatherings, and 24.3% had exposure while shopping or at a hospital. Median times of nucleic acid negative conversion in group A+B (course of disease < 3 weeks) and group C+D (course of disease ≥ 3 weeks) were 23 days and 37 days, respectively (P < 0.05). Other group comparisons, i.e., of A+C with B+D, A with B, or C with D, were not statistically different. One week after reexamination, chest CT lesion area had changed by 52% in group C and 50% in group D (P > 0.05). In some patients, administration of glucocorticoid for more than 4 weeks significantly promoted the reduction of inflammatory shadow in the lung. Conclusion: Most patients hospitalized with COVID-19 in Wuhan were middle-aged and elderly people with underlying diseases and a history of family gatherings. Glucocorticoid therapy did not affect nor prolong the duration of nucleic acid negative conversion. Glucocorticoid therapy could promote improvement of lung lesions within 3 weeks after disease onset. Beyond 3 weeks, the treatment did not promote reduction in lung shadow area, however the density of shadow did decrease.

Erratum: Study on clinical characteristics of 173 cases of COVID-19 and effect of glucocorticoid on nucleic acid negative conversion.

[This corrects the article on p. 4251 in vol. 13, PMID: 34150012.].

[Study on the mechanism of HLA-I-expressing regulation caused by the core region mutation of HBV adr subtype].

OBJECTIVE: To study the influence and mechanism of HBV core region mutation on HLA-I expression. METHODS: Eukaryotic expression vectors of HBV core region mutations L97, G87 and V60 were constructed and transfected into HepG2 cells. Then the expressions of HLA-I were detected by RT-PCR and Western blot. The mRNA of antigen-presentation-associated genes, including LMP2, TAP1 and tapasin, were measured using RT-PCR. RESULTS: Different levels of HBsAg in the supernatants of transfected cells were detected by ELISA. The HBsAg of the mutated groups was markedly higher than that of the wild ones. All the transfected cells expressed HLA-I molecules, especially the L97 group. It was also found that the mRNA of TAP1 gene was up-regulated, while the mRNA of LMP and tapasin genes had no changes. CONCLUSION: The core region mutation of HBV can lower the expression of HBsAg; mutated groups and wild ones both can increase the expression of HLA-I molecules. The up-regulation of TAP1 gene expression might be the cause of these changes.

Modulation of Tim-3 Expression by Antigen-Dependent and -Independent Factors on T Cells from Patients with Chronic Hepatitis B Virus Infection.

T-cell immunoglobulin domain and mucin domain-containing molecule-3 (Tim-3) was up-regulated on viral specific T cells and contributed to T cells exhaustion during chronic hepatitis B virus (HBV) infection. However, modulation of Tim-3 expression was still not fully elucidated. To evaluate the potential viral and inflammatory factors involved in the inductor of Tim-3 expression on T cells, 76 patients with chronic HBV infection (including 40 chronic hepatitis B [CHB] and 36 asymptomatic HBV carriers [AsC]) and 40 of normal controls (NCs) were enrolled in this study. Tim-3 expressions on CD4+ and CD8+ T cells were assessed in response to HBV-encoding antigens, HBV peptide pools, and common γ-chain (γc) cytokines stimulation by flow cytometry. HBV peptides and anti-CD3/CD28 directly induced Tim-3 expression on T cells. γc cytokines also drive Tim-3 up-regulations on both CD4+ and CD8+ T cells in patients with chronic HBV infection. However, γc cytokines did not enhance the Tim-3 inductions by either anti-CD3/CD28 or HBV peptides stimulation. Furthermore, γc cytokines-mediated Tim-3 induction could not be abrogated by γc cytokine receptor-neutralizing antibodies. The current results suggested that elevation of Tim-3 expression on T cells could be regulated by both antigen-dependent and -independent manner in patients with chronic HBV infection. The role of γc cytokines in modulation of inhibitory pathway might be evaluated as immunotherapies in humans.

The Efficacy of Add-on Telbivudine Versus Switching to Pegylated Interferon Alfa-2a in Chronic Hepatitis B Patients With Poor Responses to Adefovir.

BACKGROUND: There are limited options for chronic hepatitis B (CHB) patients who have poor responses to adefovir (ADV). OBJECTIVES: The aim of this study is to evaluate the effects of adding on telbivudine (LdT) or switching to pegylated interferon alfa-2a (PEG-IFN-α2a) as alternative rescue therapies for patients with poor responses to the initial ADV treatments. PATIENTS AND METHODS: Ninety-seven CHB patients with HBV DNA > 2 log10 copies/mL 48 weeks after ADV monotherapy were included in this study. Fifty-nine of these patients were treated with a combination of LdT plus ADV (LdT + ADV) daily, while thirty-eight patients were switched to PEG-IFN-α2a subcutaneous injections weekly for 48 weeks. RESULTS: Both rescue strategies were proven to be safe and the majority of patients tolerated the therapies well. LdT + ADV led to more rapid reductions in viral loads than PEG-IFN-α2a monotherapy, with 2.14 (LdT + ADV) and 0.98 (PEG-IFN-α2a) log10 copies/mL decreases 48 weeks after rescue treatments, respectively (P < 0.00001). The rates corresponding to virological and biochemical responses were also elevated in patients who received the LdT + ADV combination therapy at the end of the observation period (88.1 vs. 68.4% for virological response, P = 0.017; 83.3 vs. 47.2%, P = 0.00045). However, the decline in the hepatitis B surface antigen (HBsAg) was more pronounced in PEG-IFN-α2a treated patients. Moreover, the cumulative rates of serological responses were higher in patients who switched to the PEG-IFN-α2a therapy. CONCLUSIONS: Both add-on LdT and switching to PEG-IFN-α2a were satisfactory and optimal treatments for CHB patients with poor responses to ADV. Both rescue strategies resulted in significant reductions in serum viral load and ALT levels, and were associated with high rate of serological outcomes in our hospital.

Notch Signaling Contributes to Liver Inflammation by Regulation of Interleukin-22-Producing Cells in Hepatitis B Virus Infection.

The mechanism of hepatitis B virus (HBV) induced liver inflammation is not fully elucidated. Notch signaling augmented interleukin (IL)-22 secretion in CD4+ T cells, and Notch-IL-22 axis fine-tuned inflammatory response. We previously demonstrated a proinflammatory role of IL-22 in HBV infection. Thus, in this study, we analyzed the role of Notch in development of IL-22-producing cells in HBV infection by inhibition of Notch signaling using γ-secretase inhibitor DAPT in both hydrodynamic induced HBV-infected mouse model and in peripheral blood cells isolated from patients with HBV infection. mRNA expressions of Notch1 and Notch2 were significantly increased in livers and CD4+ T cells upon HBV infection. Inhibition of Notch signaling in vivo leaded to the reduction in NKp46+ innate lymphoid cells 22 (ILC22) and lymphoid tissue inducer 4 (LTi4) cells in the liver. This process was accompanied by downregulating the expressions of IL-22 and related proinflammatory cytokines and chemokines in the liver, as well as blocking the recruitment of antigen-non-specific inflammatory cells into the liver and subsequent liver injury, but did not affect HBV antigens production and IL-22 secretion in the serum. Furthermore, IL-22 production in HBV non-specific cultured CD4+ T cells, but not HBV-specific CD4+ T cells, was reduced in response to in vitro inhibition of Notch signaling. In conclusion, Notch siganling appears to be an important mediator of the liver inflammation by modulating hepatic ILC22. The potential proinflammatory effect of Notch-mediated ILC22 may be significant for the development of new therapeutic approaches for treatment of hepatitis B.

Escherichia coli surface display of single-chain antibody VRC01 against HIV-1 infection.

Human immunodeficiency virus type 1 (HIV-1) transmission and infection occur mainly via the mucosal surfaces. The commensal bacteria residing in these surfaces can potentially be employed as a vehicle for delivering inhibitors to prevent HIV-1 infection. In this study, we have employed a bacteria-based strategy to display a broadly neutralizing antibody VRC01, which could potentially be used to prevent HIV-1 infection. The VRC01 antibody mimics CD4-binding to gp120 and has broadly neutralization activities against HIV-1. We have designed a construct that can express the fusion peptide of the scFv-VRC01 antibody together with the autotransporter ß-barrel domain of IgAP gene from Neisseria gonorrhoeae, which enabled surface display of the antibody molecule. Our results indicate that the scFv-VRC01 antibody molecule was displayed on the surface of the bacteria as demonstrated by flow cytometry and immunofluorescence microscopy. The engineered bacteria can capture HIV-1 particles via surface-binding and inhibit HIV-1 infection in cell culture.

[The induced IL-21 levels in CD4(+) T cells of peripheral blood from the different clinical types of patients infected with hepatitis B virus].

AIM: To investigate the levels of interleukin (IL)-21 in CD4(+);T cells of peripheral blood from the different types of patients infected with hepatitis B virus (HBV) and elucidate its role in the hepatitis B pathogenesis. METHODS: Peripheral blood mononuclear cells (PBMCs) from the patients infected with HBV and healthy individuals were stimulated with or without PMA coupled with ionomycin. The levels of IL-21 in CD4(+) T cells and Th17 cells were analyzed by flow cytometry. RESULTS: PMA and ionomycin induced the expression of IL-21, and IL-21 was mainly produced by CD4(+); T cells, but IL-17A(+) IL-21(+) CD4(+) T cells were not detected. The frequencies of IL-21(+) CD4(+) T cells in the patients of acute hepatitis B and chronic asymptomatic HBV carriers were higher than in healthy controls and severe chronic hepatitis B patients; there were no remarkable differences in the proportion of Th17 cells among the different groups of patients. Furthermore, the proportion of IL-21(+) CD4(+) T cells correlated with Th17 cells in all groups except for the acute hepatitis B patients. CONCLUSION: IL-21 levels, which correlated with Th17 cells, were different in CD4(+);T cells from the different types of patients infected with hepatitis B virus (HBV). The results showed that IL-21 may play a role in the hepatitis B pathogenesis.

[Experimental study on immune responses induced in mice by gp120 gene vaccine of Chinese HIV-1 strain].

AIM: To construct the gp120 DNA vaccine of Chinese HIV-1 strain and evaluate the immune responses induced with it in BALB/c mice. METHODS: The recombinant expression vector pVAX1-GP120 was constructed by inserting HIV gp120 gene into the eukaryotic expression vector pVAX1 and confirmed with EcoR I/Pst I and DNA sequencing. BALB/c mice were immunized with pVAX1-GP120 and pVAX1 respectively. The levels of serum anti-HIV antibody and IFN-gamma of the immunized mice were detected by ELISA. The proliferation of splenocytes was determined by MTT colorimetry and the specific cytotoxic T lymphocytes (CTLs) response by LDH assay. RESULTS: Restriction enzymes digestion analysis and DNA sequencing results revealed that the pVAX1-GP120 had been constructed successfully. The titer of anti-HIV antibody and the IFN-gamma level in mice immunized with the pVAX1-GP120 were higher than those in mice immunized with pVAX1 respectively (P<0.01). As compared with mice immunized with pVAX1 alone, the cytotoxic activity of specific CTLs and antigen-specific lymphoproliferative responses in mice immunized with pVAX1-GP120 were significantly enhanced (P<0.01). CONCLUSION: Specific cellular and humoral immune responses in mice can be induced with gp120 gene vaccine of Chinese HIV-1 strain, which lays the foundation for further development of therapeutic HIV vaccine against HIV-1 infection.

[Inhibition of momordica anti-HIV protein of MAP30 on HBeAg expression by laser scanning confocal microscopy].

AIM: To investigate the effect of momordica anti-HIV protein of M(r ) being 30 000 (MAP30) on HBV expression by laser scanning confocal microscopy. METHODS: HBV DNA-transfected hepatocarcinoma cells 2.2.15 were cultured in the presence of MAP30. Then quantitative analysis of HBeAg expression in the 2.2.15 cells by laser scanning confocal microscopy after indirect immunofluorescence staining was performed. RESULTS: The fluorescence intensity in 2.2.15 cells co-cultured with MAP30 was notably weaker than that in control cells. CONCLUSION: MAP30 can effectively inhibit HBeAg expression in the 2.2.15 cells.