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Researchers at the National Cancer Institute (NCI) have developed a method of stimulating an immune response in humans at risk for infection by, or already infected with, an Human Immunodeficiency Virus (HIV)-1 retrovirus. This method utilizes deoxyribonucleic acid (DNA) vaccines to stimulate CD8+ T cell immune responses. The DNA vaccine encodes antigens known to be effective against retroviruses, such as HIV-1gag, gp120, nefCTL, and proCTL. The same antigens are also expressed by the pox virus vaccine, which elicits an increased immune response when combined with the DNA vaccine.

Human immunodeficiency virus (HIV) remains a major global health challenge despite the advancement made in development of effective antiretrovirals (ARVs). ARVs are effective at limiting replication and spread of the virus, and progression to acquired immuno-deficiency syndrome (AIDS). However, ARVs often lead to emergence of drug-resistant virus strains insensitive to treatment and with toxic effects following long-term usage.

Researchers at the National Cancer Institute (NCI) have developed a new method of improving the efficacy of vaccines in patients with human immunodeficiency virus (HIV) by activating Ras. This method can be used to develop more efficacious vaccine compositions by activating Ras before, during, or after vaccination. Additionally, the researchers discovered that modulation of the Ras pathways could be a predictive biomarker of protection against HIV.

This technology includes the use of thymic stromal lymphopoetin (TSLP) for the treatment of MRSA. Our studies show that mouse neutrophils express the TSLP receptor, TSLPR, and that TSLP protein is increased during cutaneous MRSA infection. Using in vitro MRSA whole blood killing assays, we show that TSLP acts on mouse neutrophils to enhance MRSA killing. In an in vivo MRSA intradermal ear infection, TSLPR-deficient mice exhibit increased MRSA burden compared to wild-type mice.

This technology includes irradiated Epstein-Barr virus-transformed lymphoblastoid cell lines (EBV-LCL) as feeder cells for the ex vivo expansion of natural killer (NK) cells. EBV-LCL feeder cells, altered by radiation to prevent uncontrolled growth, provide a supportive environment for NK cells to multiply effectively. This method addresses the challenge of obtaining sufficient quantities of functionally active NK cells, which are crucial components of the immune system known for their ability to target and destroy tumor cells and virally infected cells.

The technology described involves the use of a compound called prazole as an anti-viral agent specifically targeting HIV-1. It was found that prazole binds to a protein called Tsg101, which is crucial for the virus's life cycle. This binding disrupts the normal interaction of Tsg101 with another protein, ubiquitin, thereby inhibiting the release of HIV-1 particles from infected cells. Additionally, the interference caused by prazole leads to the degradation of the viral protein Gag within host cells.

This technology includes an IgA antibody, specifically designed to target the receptor binding domain of SARS-CoV-2, the virus causing COVID-19. Administered intranasally, this antibody has potential neutralizing activity, aiming to prevent COVID-19. IgA, an antibody class present in mucosal areas, plays a crucial role in immune defense at the initial site of viral infection. The primary application of this technology is envisioned as a therapeutic nasal spray, intended to prevent SARS-CoV-2 infection, particularly in high-risk populations.

This technology involves the utilization of highly effective nanobodies, specifically camelid antibodies, derived from immunized llamas to neutralize SARS-CoV-2. Additionally, it employs a unique mouse model, called a "nanomouse," that is engineered to express antibody genes from camels, alpacas, and dromedaries. These nanobodies offer significant advantages over traditional human and mouse antibodies due to their smaller size, which allows them to effectively target and bind to specific areas on antigens.

RNA interference (RNAi) is a naturally occurring cellular post-transcriptional gene regulation process that utilizes small double-stranded RNAs to trigger and guide gene silencing. By introducing synthetic RNA duplexes called small-interfering RNAs (siRNAs), we can harness the RNAi machinery for therapeutic gene control and the treatment of various diseases.