Provided is a host cell for stably propagating a virulent hand, foot and mouth disease virus, the host cell expressing no heparan sulfate and overexpressing primate scavenger receptor class B member 2 (SCARB2). Also provided is a method for screening for an anti-hand, foot and mouth disease virus vaccine or an anti-hand, foot and mouth disease virus drug using a stably cultured virulent hand, foot and mouth disease virus.

The present disclosure relates to recombinant RNA molecules encoding an oncolytic virus genome. The present disclosure further relates to the encapsulation of the recombinant RNA molecules and the use of the recombinant RNA molecules and/or particles for the treatment and prevention of cancer.

In a method for manufacturing a modified enterovirus of ECHO 7 type by modification of native ECHO 7 virus, isolated by a known method from human feces and identified by genome sequence, the modification is performed initially conducting the virus adaptation in cancer cells, attenuated by anti-cancer agent dacarbazine, further passaging the modified virus in human embryonal fibroblast culture, followed by propagation in human melanoma cells and further passaging in human embryonal fibroblast culture, that was treated by ribavirin, isolation and purification by known method. The modified virus is suitable for treating various tumors.

The disclosure provides a recombinant oncolytic virus, a synthetic DNA sequence and applications of the virus. The recombinant oncolytic virus includes a genome and an exogenous DNA sequence inserted in the genome. The exogenous DNA sequence adapts to express a basic peptide fragment, to increase the environmental pH in a host infected by the recombinant oncolytic virus. The basic peptide fragment includes more than 60% of basic amino acids. The recombinant oncolytic virus and the synthetic DNA sequence of the disclosure are used to prepare an anti-tumor drug.

In a method for manufacturing a modified enterovirus of ECHO 7 type by modification of native ECHO 7 virus, isolated by a known method from human feces and identified by genome sequence, the modification is performed initially conducting the virus adaptation in cancer cells, attenuated by anti-cancer agent dacarbazine, further passaging the modified virus in human embryonal fibroblast culture, followed by propagation in human melanoma cells and further passaging in human embryonal fibroblast culture, that was treated by ribavirin, isolation and purification by known method. The modified virus is suitable for treating various tumours.

The present invention relates to a method for treating cancer in a subject in need thereof, comprising administering to said subject a therapeutically effective amount of a Coxsackie B3 group virus or a modified form thereof, wherein the cells of the cancer express a heparan sulfate (HS) receptor on their surface and the virus binds to said HS receptor, enters and accumulates in the cancer cells, whereby at least some cancer cells undergo viral lysis.

A gene-modified coxsackievirus that is to be used in oncolytic virotherapy and is improved in safety and/or aggressiveness is provided. A gene-modified coxsackievirus that contains a mutated genome with a coxsackievirus B3 wild-type (CVB3-WT) genome inserted with at least one polynucleotide constituted of a target sequence for at least one of either of miR-34a and miR-34c and is suppressed in proliferation in normal cells is provided.

In a method for manufacturing a modified enterovirus of ECHO 7 type by modification of native ECHO 7 virus, isolated by a known method from human feces and identified by genome sequence, the modification is performed initially conducting the virus adaptation in cancer cells, attenuated by anti-cancer agent dacarbazine, further passaging the modified virus in human embryonal fibroblast culture, followed by propagation in human melanoma cells and further passaging in human embryonal fibroblast culture, that was treated by ribavirin, isolation and purification by known method. The modified virus is suitable for treating various tumours.

The Coxsackievirus B3 (CVB3) vaccine including a mutant strain of Coxsackievirus B3 (CVB3) (SEQ ID NO: 1) has specific double mutations introduced in the Internal Ribosome Entry Segment (IRES) region of the wild type Coxsackievirus B3 (CVB3) genome in the nucleotide positions 473 (in which uracil is substituted for cytosine) and 475 (in which cytosine is substituted for uracil). The resulting double mutant (SEQ ID NO: 1) demonstrates a significant decrease in its replicative capacity and a drastic decrease in its translation efficiency compared to the wild-type Coxsackievirus B3 (CVB3) strain.

Disclosed herein are recombinant polypeptides derived from FBP1 and FBP2. Also disclosed herein are recombinant expression vectors and recombinant host cells for producing the aforesaid recombinant polypeptides. The recombinant polypeptides are proven to be useful and effective in producing a picornavirus with a type I internal ribosome entry site (IRES), so as to facilitate the preparation of a viral vaccine.