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Adeno-associated virus (AAV) is a promising vector for human gene therapy due to its low immunogenicity and pathogenicity. AAV vectors are constructed by replacing the AAV rep and cap genes with a therapeutic gene cassette. The vector is delivered along with a helper plasmid providing rep and cap functions. Several preclinical and clinical studies have demonstrated the potential of AAV vectors for treating lung cancer, liver cancer, diabetes, and HIV/AIDS by delivering genes such as P130, E1a, Acrp30, and 2,5-dkgr. Further research is still needed but AAV shows promise as a safe and effective method for human gene therapy.
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The document discusses the roles of dendritic cells and the dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN) protein in both cis-infection and trans-infection of HIV. DC-SIGN binds to the gp120 envelope protein of HIV and allows dendritic cells to transport the virus to permissive CD4+ T cells in lymph nodes, facilitating trans-infection. Langerhans cells express the related Langerin protein instead of DC-SIGN, and transport HIV to Birbeck granules where it is degraded, thus protecting against epithelial infection in contrast to dendritic cells.
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Human Immunodeficiency Virus (HIV) infects cells by attaching to the CD4 receptor with its gp120 glycoprotein. It requires a co-receptor, CCR5 or CXCR4, for fusion and entry into the cell. Once inside, the viral RNA is converted to DNA by reverse transcriptase. The DNA integrates into the host genome with the help of integrase. The virus hijacks the cell's machinery to produce new viral proteins and RNA, which are assembled into new virus particles that bud from the cell.
Htlv 1
Transgenic mice were developed that expressed the HTLV-1 Tax gene. These mice developed several diseases resembling HTLV-1 associated human diseases like ATLL and HAM/TSP. Expression of Tax in the mature T cell compartment led to development of leukemia in mice. Local administration of anti-Fas antibody improved arthritis in HTLV-1 Tax transgenic mice, suggesting a potential new treatment for rheumatoid arthritis. IFN-gamma knockout enhanced tumor growth in HTLV-1 Tax transgenic mice, indicating IFN-gamma contributes to resistance against HTLV-1 induced tumors. IL-1 knockout suppressed arthritis development in both HTLV-1 Tax transgenic mice and collagen-induced arthritis mice, suggesting IL-1 activation of T cells
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Therapies, especially endocrine and targeted therapies, can selectively pressure tumor cells, causing shifts in receptor expression.
Heterogeneity:
Inherent heterogeneity within the tumor can result in subpopulations of cells with different receptor statuses.
Impact on Treatment:
Therapeutic Resistance:
Loss of ERα or PgR can lead to resistance to endocrine therapies.
HER2 discordance affects the efficacy of HER2-targeted treatments.
Treatment Adjustment:
Regular reassessment of receptor status may be necessary to adjust treatment strategies appropriately.
Clinical Implications:
Prognosis:
Receptor discordance is often associated with a poorer prognosis.
Biopsies:
Obtaining biopsies from metastatic sites is crucial for accurate receptor status assessment and effective treatment planning.
Monitoring:
Continuous monitoring of receptor status throughout the disease course can guide personalized therapy adjustments.
Understanding and managing receptor discordance is essential for optimizing treatment outcomes and improving the prognosis for breast cancer patients.
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