Apicomplexan parasites or red blood cells infected with apicomplexan parasites are administered to an animal in combination with a delayed death agent that initially allows parasite replication but subsequently kills the apicomplexan parasites. This allows the elicitation of an immune response by the animal while preventing the parasites producing a serious infection of the animal. The apicomplexan parasites may be malaria or babesia parasites. The delayed death agent may be a tetracycline class antibiotic, a macrolide antibiotic or a lincosamide antibiotic.

Provided herein are multivalent particles and compositions of multivalent particles for blocking viral infection.

Disclosed herein are methods for producing virus-infected cell lines or animal models, wherein an enveloped virus including a lipid bilayer is mixed with a bile acid or a bile acid derivative, which allows the lipid bilayer to be replaced with a lipid bilayer derived from a target animal. Also disclosed herein are the virus-infected cell lines or animal models so produced and methods of screening a therapeutic candidate for a viral disease using the same.

This application relates to potent oligonucleotides useful for reducing HBsAg expression and treating HBV infections.

The current invention describes a laboratory animal model for dirofilarial nematodes wherein said laboratory animal is fed a dietary admixture of laboratory feed containing an immunosuppressing agent, for example, a glucocorticoid. The invention also describes the use of the laboratory animal model for screening endoparasiticides for the treatment and/or prevention of filarial nematode infections in animals.

A method of treating at least one of septicemia, endotoxemia or a bacterial infection in a subject can include administering to the subject a composition containing a therapeutically effective amount of a haloperoxidase. The haloperoxidase can be myeloperoxidase or eosinophil peroxidase. The haloperoxidase can inhibit lipopolysaccharide or Lipid A activity in the subject; as a non-limiting example, the haloperoxidase is not engaged in active haloperoxidase activity, but available for LPS or Lipid A binding and inhibition.

The present invention relates to a porcine sodium taurocholate cotransporter polypeptide (NTCP) mutein, which has been modified at sequence positions 157-167 with the human sequence. This NTCP mutein renders a host cell and a transgenic animal susceptible for an infection with hepatitis B virus (HBV) and/or hepatitis D virus (HDV). The present invention further relates to a nucleic acid and a vector comprising the NTCP mutein of the invention. Also presented are methods for producing cells and transgenic animals, which are susceptible to HBV and/or HDV as well as uses of the NTCP mutein screening for compounds or rendering a cell susceptible for an infection with HBV and/or HDV. Additionally provided is a method for identifying a compound, which is useful in the prevention and/or treatment of HBV and/or HDV infection.

This application relates to potent oligonucleotides useful for reducing HBsAg expression and treating HBV infections.

Non-human animals comprising a human or humanized DPP4 nucleic acid sequence are provided. Non-human animals that comprise a replacement of the endogenous Dpp4 gene with a human or humanized DPP4 gene, or non-human animals comprising a human or humanized DPP4 gene in addition to the endogenous Dpp4 gene are described. Non-human animals comprising a human or humanized DPP4 gene under control of human or non-human DPP4 regulatory elements is also provided, including non-human animals that have a replacement of non-human Dpp4-encoding sequence with human DPP4-encoding sequence at an endogenous non-human Dpp4 locus. Non-human animals comprising human or humanized DPP4 gene sequences, wherein the non-human animals are rodents, e.g., mice or rats, are provided. Methods for making and using the non-human animals are described.

The present invention provides a mouse with liver damage, having a high degree of damage against the mouse's original hepatocytes while having a uPA gene in a heterozygous form, and a method for efficiently preparing the mouse. Specifically, the method for preparing a mouse with liver damage having the uPA gene in a heterozygous form comprises the following steps of: (i) transforming mouse ES cells with a DNA fragment containing a liver-specific promoter/enhancer and cDNA that encodes a urokinase-type plasminogen activator operably linked under the control thereof; (ii) injecting the transformed mouse ES cells obtained in step (i) into a host embryo; (iii) transplanting the host embryo obtained in step (ii) via the injection of the ES cells into the uterus of a surrogate mother mouse, so as to obtain a chimeric mouse; and (iv) crossing the chimeric mice obtained in step (iii), so as to obtain a transgenic mouse in which the DNA fragment is introduced in a heterozygous form.