Abstract: The present invention relates to cobicistat and its derivatives or prodrugs for use in the prophylaxis and/or treatment of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) infection, severe acute respiratory syndrome coronavirus (SARS-CoV) infection and/or Middle East respiratory syndrome coronavirus (MERS-CoV) infection. The present invention further relates to methods of prevention and/or treatment of SARS-CoV-2 infection.

Abstract: Computational prediction of immunogenic epitopes is a promising platform for designing therapeutic and preventive vaccines. A potential target is, for example, the human immunodeficiency virus (HIV-1) for which, despite decades of efforts, no vaccine is available. Indeed, due to the enormous variability of the virus, a single formulation effective against all or most HIV strains might not be achievable. Moreover, upon infecting host cells, HIV-1 can integrate in the host genome and form long lasting latent reservoirs that are not susceptible to common antiretroviral treatments. Therefore, a therapeutic vaccine designed to eliminate infected cells might represent a key component of strategies aimed at curing the infection. We herein introduce an automated algorithm to produce personalized and population-based vaccines.

Abstract: A novel approach to the development of a personalized vaccine. This approach is based on: A) sequencing of the gag gene from an HIV-infected individual treated with antiretroviral therapy; B) sequencing of the HLA alleles of the same individual; C) selecting the epitopes recognized by the individual's own HLA Class I within the highly-conserved Gag256-377, Gag147-169 and/or Gag225-251 amino acid sequences. An original algorithm that designs the target peptide for the vaccine starting from viral and HLA sequences of an individual with HIV/AIDS, forms the core of the present invention. The original algorithm makes extensive use of existing open- source software for protein design. The peptides designed in this manner and accordingly synthesized may be exploited as a therapeutic vaccine against HIV/AIDS. Vehicles for such peptides may be an individual's own dendritic cells pulsed with the peptide combination or a specific viral or DNA vector leading to intracellular expression of the viral peptides.

Abstract: There is disclosed buthionine sulfoximine (BSO) for use in a method of treatment of cancer, HIV or a rheumatic disease. The method comprises administering (a) BSO at a dosage of less than or equal to 50 mg/kg, and (b) a metallodrug at a clinically-acceptable dosage.

Abstract: There is disclosed buthionine sulfoximine (BSO) for use in a method of treatment of cancer, HIV or a rheumatic disease. The method comprises administering (a) BSO at a dosage of less than or equal to 50 mg/kg, and (b) a metallodrug at a clinically-acceptable dosage.

Abstract: There is disclosed buthionine sulfoximine (BSO) for use in a method of treatment of cancer, HIV or a rheumatic disease. The method comprises administering (a) BSO at a dosage of less than or equal to 50 mg/kg, and (b) a metallodrug at a clinically-acceptable dosage.

Abstract: Activation of HIV-1 replication causes oxidative stress, which in turn potentiates HIV-1 replication. The common basis for the compounds of the present invention is: A) the capacity of reactivating HIV-1 from latency, and B) the ability to counteract the cellular machinery which activates in order to limit the effects of oxidative stress. In this way, oxidative stress can be potentiated and a “chain reaction” is sparked. This “chain reaction” induces a more efficient reactivation of HIV-1 from latency and, in some cases, induces selective killing of the infected cells. Actions A) and B) can either be carried out by one drug exerting both effects, or obtained by the combined use of distinct drugs. There are two main cellular machineries counteracting oxidative stress, i.e. the thioredoxin (Trx) thioredoxin reductase (TrxR) system and glutathione. Herein, we present drug strategies capable of exerting action B) by blocking either of the two machineries.

Abstract: Activation of HIV-1 replication causes oxidative stress, which in turn potentiates HIV-1 replication. The common basis for the compounds of the present invention is: A) the capacity of reactivating HIV-1 from latency, and B) the ability to counteract the cellular machinery which activates in order to limit the effects of oxidative stress. In this way, oxidative stress can be potentiated and a “chain reaction” is sparked. This “chain reaction” induces a more efficient reactivation of HIV-1 from latency and, in some cases, induces selective killing of the infected cells. Actions A) and B) can either be carried out by one drug exerting both effects, or obtained by the combined use of distinct drugs. There are two main cellular machineries counteracting oxidative stress, i.e. the thioredoxin (Trx) thioredoxin reductase (TrxR) system and glutathione. Herein, we present drug strategies capable of exerting action B) by blocking either of the two machineries.

Abstract: Activation of HIV-1 replication causes oxidative stress, which in turn potentiates HIV-1 replication. The common basis for the compounds of the present invention is: A) the capacity of reactivating HIV-1 from latency, and B) the ability to counteract the cellular machinery which activates in order to limit the effects of oxidative stress. In this way, oxidative stress can be potentiated and a “chain reaction” is sparked. This “chain reaction” induces a more efficient reactivation of HIV-1 from latency and, in some cases, induces selective killing of the infected cells. Actions A) and B) can either be carried out by one drug exerting both effects, or obtained by the combined use of distinct drugs. There are two main cellular machineries counteracting oxidative stress, i.e. the thioredoxin (Trx) thioredoxin reductase (TrxR) system and glutathione. Herein, we present drug strategies capable of exerting action B) by blocking either of the two machineries.

Abstract: Peptides representing sequences from region 45-74 of the human CD38 leukocyte surface antigen (SEQ ID NO:1) are provided which may be used to inhibit or prevent transmission or replication of the HIV virus. The peptides have from 13 to 30 amino acids and include the amino acid sequence GPGTTK (SEQ ID NO:18) for topical application to inhibit or prevent transmission of the HIV virus.

Abstract: Activation of HIV-1 replication causes oxidative stress, which in turn potentiates HIV-1 replication. The common basis for the compounds of the present invention is: A) the capacity of reactivating HIV-1 from latency, and B) the ability to counteract the cellular machinery which activates in order to limit the effects of oxidative stress. In this way, oxidative stress can be potentiated and a “chain reaction” is sparked. This “chain reaction” induces a more efficient reactivation of HIV-1 from latency and, in some cases, induces selective killing of the infected cells. Actions A) and B) can either be carried out by one drug exerting both effects, or obtained by the combined use of distinct drugs. There are two main cellular machineries counteracting oxidative stress, i.e. the thioredoxin (Trx) thioredoxin reductase (TrxR) system and glutathione. Herein, we present drug strategies capable of exerting action B) by blocking either of the two machineries.

Abstract: Peptides representing sequences from region 45-74 of the human CD38 leukocyte surface antigen (SEQ ID NO:1) are provided which may be used to inhibit or prevent transmission or replication of the HIV virus. The peptides have from 13 to 30 amino acids and include the amino acid sequence GPGTTK (SEQ ID NO:18) for topical application to inhibit or prevent transmission of the HIV virus.

Abstract: The invention relates to cell lines from differentiated cells with hepatocytic phenotypes capable of producing albumin and blood coagulation factors, said cells being derived from a human leukaemia cell line, preferably the human THP1 cell line, and preserving the characteristics of immortality. Among the cell lines of the invention, the cell lines known as PSC-THP1-EP, PSC-THP1-EP-FAST, PSC-THP1-HEP and PSC-THP1-EPEP are preferred. The invention also relates to methods for obtaining the cell lines of the invention and the uses of said cell lines, particularly for the production of albumin and/or blood coagulation factors.

Abstract: The present invention relates to a drug combination capable of conferring therapeutic benefits in the treatment of both AIDS and malaria. In particular, it relates to a drug combination including at least one quinolinic antimalarial compound such as chloroquine or hydroxychloroquine, and at least one inhibitor of the Human Immunodeficiency Virus (HIV) protease enzyme. This drug combination is capable of inhibiting the replication of both HIV and Plasmodium sp. It also relates to the direct antimalarial effects of the HIV PIs.

Abstract: Peptides representing sequences from region 45-74 of the human CD38 leukocyte surface antigen are provided which may be used to inhibit or prevent transmission or replication of the HIV virus. The peptides have from 13 to 30 amino acids and include the amino acid sequence GPGTTK (SEQ ID for topical application to inhibit or prevent transmission of the HIV virus.

Abstract: The present invention relates to a drug combination capable of conferring therapeutic benefits in the treatment of both AIDS and malaria. In particular, it relates to a drug combination including at least one quinolinic antimalarial compound such as chloroquine or hydroxychloroquine, and at least one inhibitor of the Human Immunodeficiency Virus (HIV) protease enzyme. This drug combination is capable of inhibiting the replication of both HIV and Plasmodium sp. It also relates to the direct antimalarial effects of the HIV PIs.

Abstract: Peptides representing sequences from region 45-74 of the human CD38 leukocyte surface antigen (SEQ ID NO:1) are provided which may be used to inhibit or prevent transmission or replication of the HIV virus. The peptides have from 13 to 30 amino acids and include the amino acid sequence GPGTTK (SEQ ID NO:18) for topical application to inhibit or prevent transmission of the HIV virus.

Abstract: Peptides representing sequences from region 45-74 of the human CD38 leukocyte surface antigen (SEQ ID NO:1) are provided which may be used to inhibit or prevent transmission or replication of the HIV virus. The peptides have from 13 to 30 amino acids and include the amino acid sequence GPGTTK (SEQ ID NO:18) for topical application to inhibit or prevent transmission of the HIV virus.

Abstract: The present invention relates to immortal pluripotent stem cells derived from a human leukaemia cell line, preferably a human monocytoid cell line and more preferably the human monocytoid cell line, THP1. The present invention further relates to cell lines derived from the immortal pluripotent stem cell line having the phenotype of cell strains characteristic of human tissues, particularly having a human hepatocyte phenotype, as well as the methods for preparing thereof. The present invention further relates to the use of the derived cell line with a human hepatocytic phenotype for the production of albumin and blood coagulation factors.

Abstract: The present invention relates to a drug combination capable of conferring therapeutic benefits in the treatment of both AIDS and malaria. In particular, it relates to a drug combination including at least one quinolinic antimalarial compound such as chloroquine or hydroxychloroquine, and at least one inhibitor of the Human Immunodeficiency Virus (HIV) protease enzyme. This drug combination is capable of inhibiting the replication of both HIV and Plasmodium sp. It also relates to the direct antimalarial effects of the HIV PIs.