Effect of hydrogen sulphide on inflammatory factors of the mitochondria after limb ischaemia-reperfusion injury in rats.

The goal of this study was to evaluate the effect of hydrogen sulphide on inflammatory factors and the energy metabolism of mitochondria after limb reperfusion injury in rats. Sixty Wistar rats were divided into three groups: the sham operated group, the control group (the ischaemia-reperfusion injury [IRI] + normal saline group), and the experimental group (the IRI + H2 S group). An experimental rat model of limb IRI was established. Skeletal muscle samples were collected to observe the content of necrotic products (including myoglobin (MB), lysophosphatidylcholine (LPC), and lipid peroxidation (LPO)); blood samples were collected to observe changes in the contents of interleukin-1 (IL-1), Interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α); and the mitochondria of skeletal muscle cells were extracted for mitochondrial transmembrane potential measurement and adenosine triphosphate (ATP) content determination. The results underwent further statistical analysis. The contents of MB, LPC, and LPO in the limb skeletal muscle, liver, lung, and kidney tissues of rats in the control group were significantly increased (P < 0.05) after IRI, which was markedly attenuated by treatment with hydrogen sulphide (P < 0.05). Ischaemia/reperfusion of the lower extremities in rats triggered a significant increase in serum levels of IL-1, IL-6, and TNF-α, which was significantly inhibited by treatment with H2 S during ischaemia/reperfusion. In addition, the inhibitory effect tended to be time-dependent. After limb ischaemia/reperfusion, the mitochondrial transmembrane potential of skeletal muscle cells in the control group decreased significantly (P < 0.05), while the potential energy of the mitochondrial membrane in the experimental group was significantly higher than that in the control group (P < 0.05). The content of ATP in mitochondria of skeletal muscle cells of ischaemia-reperfusion rats in the control group was significantly lower than that in the sham operated group (P < 0.05), while the content of ATP of mitochondria in the experimental group after H2 S treatment was significantly higher than the control group (P < 0.05). Hydrogen sulphide can alleviate the injury of skeletal muscle and distal organs after limb ischaemia-reperfusion and reduce local inflammatory reaction, which is essential in alleviating mitochondrial transmembrane potential and energy metabolism disorder during reperfusion injury. The purpose of the study is to summarise the available information and provide theoretical support for the application of hydrogen sulphide in the treatment of limb IRI in skeletal muscle and distal organs.

SPDEF inhibits prostate carcinogenesis by disrupting a positive feedback loop in regulation of the Foxm1 oncogene.

SAM-pointed domain-containing ETS transcription factor (SPDEF) is expressed in normal prostate epithelium. While its expression changes during prostate carcinogenesis (PCa), the role of SPDEF in prostate cancer remains controversial due to the lack of genetic mouse models. In present study, we generated transgenic mice with the loss- or gain-of-function of SPDEF in prostate epithelium to demonstrate that SPDEF functions as tumor suppressor in prostate cancer. Loss of SPDEF increased cancer progression and tumor cell proliferation, whereas over-expression of SPDEF in prostate epithelium inhibited carcinogenesis and reduced tumor cell proliferation in vivo and in vitro. Transgenic over-expression of SPDEF inhibited mRNA and protein levels of Foxm1, a transcription factor critical for tumor cell proliferation, and reduced expression of Foxm1 target genes, including Cdc25b, Cyclin B1, Cyclin A2, Plk-1, AuroraB, CKS1 and Topo2alpha. Deletion of SPDEF in transgenic mice and cultures prostate tumor cells increased expression of Foxm1 and its target genes. Furthermore, an inverse correlation between SPDEF and Foxm1 levels was found in human prostate cancers. The two-gene signature of low SPDEF and high FoxM1 predicted poor survival in prostate cancer patients. Mechanistically, SPDEF bound to, and inhibited transcriptional activity of Foxm1 promoter by interfering with the ability of Foxm1 to activate its own promoter through auto-regulatory site located in the -745/-660 bp Foxm1 promoter region. Re-expression of Foxm1 restored cellular proliferation in the SPDEF-positive cancer cells and rescued progression of SPDEF-positive tumors in mouse prostates. Altogether, SPDEF inhibits prostate carcinogenesis by preventing Foxm1-regulated proliferation of prostate tumor cells. The present study identified novel crosstalk between SPDEF tumor suppressor and Foxm1 oncogene and demonstrated that this crosstalk is required for tumor cell proliferation during progression of prostate cancer in vivo.

Association between glutathione S-transferase M1 null genotype and risk of gallbladder cancer: a meta-analysis.

Glutathione S-transferases (GSTs) are a family of enzymes which are involved in the detoxification of potential carcinogens. Glutathione S-transferase M1 (GSTM1) null genotype can impair the enzyme activity of GSTs and is suspected to increase the susceptibility to gallbladder cancer. Previous studies investigating the association between GSTM1 null genotype and risk of gallbladder cancer reported inconsistent findings. To quantify the association between GSTM1 null genotype and risk of gallbladder cancer, we performed a meta-analysis of published studies. We searched PubMed, Embase, and Wanfang databases for all possible studies. We estimated the pooled odds ratio (OR) with its 95% confidence interval (95% CI) to assess the association. Meta-analysis of total included studies showed that GSTM1 null genotype was not associated with gallbladder cancer risk (OR = 1.13, 95% CI 0.88-1.46, P = 0.332). Subgroup analysis by ethnicity showed that there was no association between GSTM1 null genotype and risk of gallbladder cancer in both Caucasians and Asians. However, meta-analysis of studies with adjusted estimations showed that GSTM1 null genotype was associated with increased risk of gallbladder cancer (OR = 1.46, 95% CI 1.02-2.09, P = 0.038). Thus, this meta-analysis shows that GSTM1 null genotype is likely to be associated with risk of gallbladder cancer. More studies with well design and large sample size are needed to further validate the association between GSTM1 null genotype and gallbladder cancer.

Rectal NSAIDs for the prevention of post-ERCP pancreatitis: a meta-analysis of randomized controlled trials.

BACKGROUND AND PURPOSE: Acute pancreatitis is the most frequent complication of endoscopic retrograde cholangiopancreatography (ERCP). We conducted a meta-analysis to evaluate the efficacy and safety of rectal nonsteroidal anti-inflammatory drugs (NSAIDs) for the prevention of post-ERCP pancreatitis (PEP). METHODS: PubMed and Embase databases were searched through April 2013. Results are reported as relative risk (RR) or weighted mean difference (WMD) with 95% confidence interval (95% CI). The primary outcome measure was the incidence of PEP. Secondary outcome measures included the severity of PEP and serum amylase level 2 h, 24 h after ERCP. RESULTS: Seven trials containing 1846 patients were eligible. Rectal NSAIDs significantly reduced the incidence of PEP (RR 0.45, 95% CI 0.34-0.61, P < 0.001). The results were maintained in subsequent subgroup analysis. Rectal NSAIDs also was associated with a reduction in the incidence of mild PEP (RR 0.54, 95% CI 0.35-0.83, P = 0.005), moderate to severe PEP (RR 0.39, 95% CI 0.22-0.70, P = 0.002), or serum amylase level 2 h after ERCP (WMD -91.09 IU/L, 95% CI -149.78 to -32.40, P = 0.002). CONCLUSIONS: Rectal NSAIDs reduced the incidence and severity of PEP, as well as serum amylase level 2 h after ERCP.

Reduction of polyhedrin mRNA and protein expression levels in Sf9 and Hi5 cell lines, but not in Sf21 cells, infected with Autographa californica multiple nucleopolyhedrovirus fp25k mutants.

During cell infection, the fp25k gene of baculoviruses frequently mutates, producing the few polyhedra (FP) per cell phenotype with reduced polyhedrin (polh) expression levels compared with wild-type baculoviruses. Here we report that the fp25k gene of the model baculovirus, Autographa californica multiple nucleopolyhedrovirus (AcMNPV), contains two hypermutable seven-adenine (A7) mononucleotide repeats (MNRs) that were mutated to A8 MNRs and a TTAA site that had host DNA insertions, producing fp25k mutants during Sf21 cell infection. The FP phenotype in Sf9 and Hi5 cells was more pronounced than in Sf21 cells. AcMNPV fp25k mutants produced similar levels of polyhedra or enhanced GFP, which were both under the control of the AcMNPV polh promoter for expression, in Sf21 cells but lower levels in Sf9 and Hi5 cells compared with AcMNPV with an intact fp25k gene. This correlated with the polh mRNA levels detected in each cell line. The majority of Sf21 cells infected with fp25 mutants showed high polh promoter-mediated GFP expression levels. Two cell lines subcloned from Sf21 cells that were infected with fp25k mutants showed different GFP expression levels. Furthermore, a small proportion of Hi5 cells infected with fp25k mutants showed higher production of polyhedra and GFP expression than the rest, and the latter was not correlated with increased m.o.i. Therefore, these data suggest that AcMNPV polh promoter-mediated gene expression activities differ in the three cell lines and are influenced by different cells within the cell line.

Cell-dependent production of polyhedra and virion occlusion of Autographa californica multiple nucleopolyhedrovirus fp25k mutants in vitro and in vivo.

Members of the family Baculoviridae are insect-specific dsDNA viruses that have been used for biological control of insect pests in agriculture and forestry, as well as in research and pharmaceutical protein expression in insect cells and larvae. Autographa californica multiple nucleopolyhedrovirus (AcMNPV) is the type species of the family Baculoviridae. During infection of AcMNPV in permissive cells, fp25k mutants are positively selected, leading to the formation of the few polyhedra (FP) phenotype with reduced yield of polyhedra and reduced virion occlusion efficiency, which leads to decreased oral infectivity for insects. Here we report that polyhedra of AcMNPV fp25k mutants produced from different insect cell lines and insects have differences in larval per os infectivity, and that these variations are due to different virion occlusion efficiencies in these cell lines and insects. Polyhedra of AcMNPV fp25k mutants produced from Sf cells (Sf21 and Sf9, derived from Spodoptera frugiperda) and S. frugiperda larvae had poorer virion occlusion efficiency than those from Hi5 cells (derived from Trichoplusia ni) and T. ni larvae, based on immunoblots, DNA isolation and larval oral infection analysis. AcMNPV fp25k mutants formed clusters of FP and many polyhedra (MP) in the fat body cells of both T. ni and S. frugiperda larvae. Transmission electron microscopy revealed that the nature of virion occlusion of AcMNPV fp25k mutants was dependent on the different cells of the T. ni fat body tissue. Taken together, these results indicate that the FP phenotype and virion occlusion efficiency of fp25k mutants are influenced by the host insect cells.

Genome of Thysanoplusia orichalcea multiple nucleopolyhedrovirus lacks the superoxide dismutase gene.

Thysanoplusia orichalcea multiple nucleopolyhedrovirus (ThorMNPV) has high virulence to Trichoplusia ni and Pseudoplusia includens larvae, with a potential for biological control of insect pests. The genome of ThorMNPV was sequenced and found to be 132,978 bp, with a G+C content of 37.9%. There are 145 predicted open reading frames (ORFs), encoding proteins of 50 or more amino acid residues with minimal overlap. Of the 145 ORFs, 141 appeared to be homologous to those of Autographa californica MNPV (AcMNPV). In comparison to AcMNPV, 9 ORFs of AcMNPV were absent in ThorMNPV, including the superoxide dismutase (sod) gene.

AcMNPV enhances infection by ThorNPV in Sf21 cells and SeMNPV in Hi5 cells.

An expression cassette containing the DsRed2 gene, which encodes the red fluorescent protein (RFP), was inserted into the wide-host-range Autographa californica M nucleopolyhedrovirus (AcMNPV) at the polyhedrin locus (vAcDsRed2). An expression cassette containing the enhanced green fluorescent protein (EGFP) gene was inserted at the gp37 locus of the narrow-host-range Thysanoplusia orichalcea MNPV (ThorMNPV) and the p10 locus of Spodoptera exigua MNPV (SeMNPV) to produce vThGFP and vSeGFP, respectively. vThGFP and vSeGFP are poor at infecting Sf21 and Hi5 cells, respectively, whereas vAcDsRed2 is highly infectious to both cell lines. During co-infection, vAcDsRed2 enhanced vThGFP infection in Sf21 cells by approximately 20-fold, and it enhanced vSeGFP infection in Hi5 cells by more than 300-fold, as detected by fluorescence measurements. In contrast, vThGFP reduced vAcDsRed2 infection by 5.4-fold in Sf21 cells, while vSeGFP reduced vAcDsRed2 by 3.2-fold in Hi5 cells. Plaque assay data did not suggest viral recombination, but vThGFP plaques surrounded by vAcDsRed2 plaques were observed. A viral DNA replication assay performed by real-time quantitative PCR suggested that the detected fluorescence correlated with virus replication. Sf21 cells infected with vAcDsRed2 were resistant to superinfection by viruses of the same type expressing EGFP (vAcGFP). These results demonstrated that AcMNPV could enhance replication of ThorMNPV and SeMNPV in non-permissive cells without recombination.

Somatosensory evoked potential changes and decompression timing for spinal cord function recovery and evoked potentials in rats with spinal cord injury.

OBJECTIVE: The study aimed to evaluate changes of somatosensory evoked potentials and the effects of decompression timing on spinal cord recovery and evoked potentials by measuring the somatosensory evoked potentials of rats with spinal cord injury at different time points. METHODS: A total of 70 SD rats were divided into the control group (group A) and the experimental group. The experimental groups included group B-D according to the severity of spinal cord injury. Somatosensory evoked potentials were evaluated in the 4 study groups after the spinal cord was opened and spinal anesthesia. Continuous operations were performed to establish the rat models of spinal cord injury until surgical trauma was detected for stable somatosensory evoked potentials. The somatosensory evoked potentials of rats were determined before injury, and 5 min, 1 and 6 h, 3 and 7 days after injury. Evoked potentials were measured before decompression, and 5 min, 1 and 6 h, 3 and 7 days after decompression in the rat models. Latency and amplitude were determined. RESULTS: There was no significant change in latency and amplitude of somatosensory evoked potentials before and after anesthesia and operation in the control group (P > 0.05). At 1 and 6 h after spinal cord injury, the more severe the spinal cord were hit, the more significant extension and decreases were observed in latency and in amplitude, respectively. Significant changes were identified in latency and vibration amplitude at 5 min after spinal cord injury in group B, C, and D than before injury with even more obvious changes in amplitude. The latency and amplitude of the somatosensory evoked potentials in the control group and each spinal cord injury group had great difference before increasing the spinal cord injury. The rats in the 30-minute compression group had significant longer latency than those in other groups after 7 days of compression; the somatosensory evoked potential amplitude recovered faster in rats with less time for compression. The wave amplitude was significantly lower in rats with 30 min' compression than that in the other groups after 7 days. CONCLUSIONS: Somatosensory evoked potential can well reflect the severity of spinal cord injury. The longer the spinal cord was compressed, the more significant were changes in somatosensory evoked potential. Changes in the amplitude of somatosensory evoked potential following spinal cord injury are more sensitive than latency changes for early diagnosis and prompt assessment of spinal cord injury.

Tau protein function: The mechanical exploration of axonal transport disorder caused by persistent pressure in dorsal root ganglia.

OBJECTIVE: We analyzed the function of Tau protein to explore the underlying mechanism of axonal transport disorder caused by persistent pressure in the dorsal root ganglia (DRG). METHODS: Wistar rats were divided into the sham operated group, the control group and the experimental group. The Wistar rat model of continuous compression of DRG was used for further investigation. DRG neurons were extracted and cultured, and the protein content was detected using bicinchoninic acid method. Western blotting and immunofluorescence assays were performed to detect the protein content. Intraperitoneal injection of lithium chloride was performed for interaction with Tau. The results were then analyzed statistically. RESULTS: After 2 weeks of sustained pressure, the expression level of Tau396 increased by 33%, while Tau404 increased by 25% in the DRG of the experimental group (p < 0.05). The expression level of PSD-95 in the DRG decreased by 15% (p < 0.05), while the expression of vGluT1, vGluT3 and vAchT decreased significantly in the DRG of the experimental group (p < 0.05). There was no significant difference in the expression of vGluT2 and vGAT among the three groups (p > 0.05). After intervention with lithium chloride, the expression of phosphorylated Tau at the above sites decreased in varying degrees compared with the model group. The expression level of Tau404 was reduced by 55%, and that of Tau199 by 60% in the DRG of the experimental group. CONCLUSION: Chronic compression of DRG and hypoxia caused phosphorylation of Tau in axons and inhibition of PSD-95, and the function of the synaptic glutamic acid vesicle is defective in the synapse. This process is crucial in the development and progression of axonal transport dysfunction induced by chronic DRG compression, and phosphorylation of Tau plays a substantial role in this process.

The protection of acute spinal cord injury by subarachnoid space injection of Danshen in animal models.

CONTEXT/OBJECTIVE: Following acute spinal cord injury (ASCI) in rabbits, subarachnoid space injection of Danshen was performed to protect the neurological damage. In this study, we established rabbit models of spinal cord injury using a modified Allen's method. DESIGN: After the operation introducing the injuries, the rabbits were randomized into two different groups, control group (normal saline, NS) and Danshen, a component extracted from Chinese herb, treatment group. Each rabbit was supplied with either the drug or placebo at 0.3 ml/kg each day through subarachnoid cavity. SETTING: Rabbit model of acute spinal cord injury were used for the response to Danshen treatment. PARTICIPANTS: Total 48 Chinese rabbits aged four∼ five months old provided by Experimental Animal Center of Hubei Province were used for this study. INTERVENTIONS: Danshen drug or placebo was administered via a silicon tube embedded under the spinal dura mater to administer the drugs into subarachnoid cavity. OUTCOME MEASURES: After the treatment, damage indicators including cell apoptosis, morphological changes and oxidative damages were assessed. RESULTS: We found out that cell apoptosis was decreased after Danshen injection as determined by downregulation of apoptosis index (AI) by TUNEL analysis as well as propidium iodide (PI) percentage by FACS analysis. In the meanwhile, we observed cells after the treatment have increased numbers of BCL-2 positive cells, this indicated the antiapoptotic gene expression is increased after Danshen treatment. When we check the oxidative damage indicators, we found superoxide dismutase (SOD) was increased and malondiadehyde (MDA) levels were decreased after the treatment. CONCLUSION: Danshen can protect ASCI through inhibition of oxidative damage in the injured cells and thus reduce the subsequent cell apoptosis in the spinal.

MiR-29b reverses oxaliplatin-resistance in colorectal cancer by targeting SIRT1.

Oxaliplatin is a commonly used chemotherapeutic drug for the treatment of advanced colorectal cancer. However, acquired drug resistance against oxaliplatin remains a major obstacle for efficient use of it, and mechanisms underlying oxaliplatin resistance are still required to be explored. In the present study, we exposed colorectal cancer cell line SW480 to oxaliplatin for a long time to obtain oxaliplatin-resistant colorectal cancer cell model (OR-SW480). We found that intracellular expression of miR-29b was decreased when the SW480 cells became oxaliplatin-resistant. More importantly, overexpression of miR-29b resensitized OR-SW480 cells to oxaliplatin treatment. Mechanically, gene of SIRT1 was identified to be the target of miR-29b. Overexpression of miR-29b in oxaliplatin-treated OR-SW480 decreased the expression of SIRT1 to enhance the ROS production and JNK phosphorylation, and thus promoting apoptosis via activation of caspase 9, 7 and 3. On the other hand, expression plasmid of SIRT1, N-acetyl cysteine or SP600125 (JNK specific inhibitor) abolished the effect of miR-29b on oxaliplatin-treated OR-SW480. We therefore demonstrated that miR-29b reverses oxaliplatin-resistance in colorectal cancer by targeting SIRT1/ROS/JNK pathway.

Effect of icariin on fracture healing in an ovariectomized rat model of osteoporosis.

Osteoporosis is frequently asymptomatic, presenting a significant clinical and economic burden, particularly following an osteoporosis-associated fracture. Icariin has been reported to inhibit osteoporosis in vitro, and the present study investigated whether icariin also promoted bone fracture healing in ovariectomized osteoporotic (OVX) rats in vivo. A total of 30 female rats were randomly divided into three groups (n=10 per group): i) Sham surgery; ii) OVX; and iii) OVX with icariin (OVX + ICA) groups. At 3 months after the ovariectomy, a unilateral cross-tibia fracture was made at the proximal right tibia. Animals were then sacrificed after 5 weeks of oral treatment. X-rays were taken at 1 week, 3 weeks and 5 weeks of treatment, and dual energy X-ray absorptiometry was used to measure the bone mineral density (BMD). Changes to the osteocalcin (BGLAP), alkaline phosphatase (ALP), tartrate-resistant acid phosphatase (TRAP) and estradiol levels in blood were measured. Callus formation and bone union were observed, the BMD was significantly higher and the BGLAP, ALP and TRAP levels were reduced, but no significant increase was observed in the blood estradiol level in the OVX + ICA group compared with the OVX group. The present findings indicate that icariin has potential as a novel alternative therapeutic agent for fracture healing in postmenopausal osteoporosis.

Salvia miltiorrhiza prevents deep vein thrombosis via antioxidative effects in endothelial cells.

Deep vein thrombosis (DVT) is a common clinical problem, which represents a significant clinical and economic burden. The present study investigated whether Salvia miltiorrhiza (S. miltiorrhiza) could prevent DVT. A total of 30 rabbits were randomly divided into three groups (n=10 per group): The control, model and Salvia groups. A ligation model was used, where the femoral veins of rabbits were exposed and ligated. Measurements of coagulation function, blood rheological parameters, antioxidative function and effects on endothelial cells were conducted. Treatment with S. miltiorrhiza one week prior to generation of the ligation model did not affect the coagulation function much, except to increase the prothrombin time. There was a statistically significant difference (P<0.05) in whole blood viscosity (1/s, 5/s, 30/s) on the third and seventh days (1/s, 5/s, 30/s and 200/s) following generation of the model. S. miltiorrhiza exhibited promising antioxidative effects, as demonstrated by a significant decrease in malondialdehyde content (P<0.05), and an increase in the activities of superoxide dismutase (P<0.05), as compared with the model group. S. miltiorrhiza was also shown to protect the vascular endothelial cells, as compared with the model group. These results suggest that S. miltiorrhiza may have potential applications for the treatment of DVT.

Short-term clinical outcomes of 42 cases of arthroscopic meniscectomy for discoid lateral meniscus tears.

Discoid lateral meniscus of the knee causes a high morbidity in China. Since the traditional treatment to open the capsule and resect the meniscus often results in arthritis, it is now believed that a discoid lateral meniscus should be treated with arthroscopy to preserve part of the meniscus. The current study aimed to investigate the short-term clinical outcomes of arthroscopic meniscectomy for the treatment of discoid lateral meniscus tears. In the present study, we diagnosed and treated 42 patients (47 knees) with discoid lateral meniscus tears using arthroscopy between February, 2007 and December, 2010. Thirty-seven knees received partial resection of the discoid meniscus, 8 received hypo-complete resection and 2 received complete resection. Thirty-nine of the patients were followed up for a mean of 21 months (ranging from 9 to 53 months). The Lysholm scoring system was used to assess the knee function prior to surgery and during the follow-up. The results were analyzed using a Student's t-test with SPSS 12.0. Our study showed that patients with treated knees returned to normal activities within 4-6 weeks, and knee functions were more improved at 9 months after operation than 3 months, as measured by the Lysholm score (P<0.05). Arthroscopic meniscectomy is an effective treatment for discoid menisci resulting in minimal invasion, quick recovery and early functional exercise. The use of arthroscopy during surgery aids to preserve the meniscus and to reduce stress, therefore, having a beneficial effect on short-term clinical outcomes.

Phylogenetic position and replication kinetics of Heliothis virescens ascovirus 3h (HvAV-3h) isolated from Spodoptera exigua.

Insect-specific ascoviruses with a circular genome are distributed in the USA, France, Australia and Indonesia. Here, we report the first ascovirus isolation from Spodoptera exigua in Hunan, China. DNA-DNA hybridization to published ascoviruses demonstrated that the new China ascovirus isolate is a variant of Heliothis virescens ascovirus 3a (HvAV-3a), thus named HvAV-3h. We investigated the phylogenetic position, cell infection, vesicle production and viral DNA replication kinetics of HvAV-3h, as well as its host-ranges. The major capsid protein (MCP) gene and the delta DNA polymerase (DNA po1) gene of HvAV-3h were sequenced and compared with the available ascovirus isolates for phylogenetic analysis. This shows a close relationship with HvAV-3g, originally isolated from Indonesia, HvAV-3e from Australia and HvAV-3c from United States. HvAV-3h infection induced vesicle production in the SeE1 cells derived from S. exigua and Sf9 cells derived from S. frugiperda, resulting in more vesicles generated in Sf9 than SeE1. Viral DNA replication kinetics of HvAV-3h also demonstrated a difference between the two cell lines tested. HvAV-3h could readily infect three important insect pests Helicoverpa armigera (Hübner), Spodoptera exigua (Hübner) and Spodoptera litura (Fabricius) from two genera in different subfamilies with high mortalities.