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- BookEric O. Freed, editor.Summary: Over the past decade, enormous progress has been made in understanding the late events in the HIV replication cycle. This has been made possible by major advances in cell biology, virology, and structural biology. The field continues to move forward rapidly, with important new discoveries being reported on a regular basis. The impact of this progress across a broad spectrum of biomedical research has been substantial. The increase in basic knowledge in the areas of HIV assembly, release, and maturation has been accompanied by new possibilities for therapeutic intervention.The work includes topics relating to basic molecular biology, cell biology, and structural biology of HIV assembly, coupled with more applied ideas of how this basic information can inform the field of antiretroviral research. The book covers all major topics pertaining to the late stages of HIV replication, with leaders in each area recruited to contribute chapters in their areas of expertise . The topics will be sufficiently focused to allow authors the opportunity to cover the latest developments in detail.
Contents:
Structural Biology of HIV Assembly
Cellular Trafficking Mechanisms in the Assembly and Release of HIV
Packaging of the HIV-1 RNA Genome
Synthesis of Functional and Variable HIV-1 Envelope Glycoproteins
HIV-1 Budding
HIV-1 Maturation
Cell-to-Cell Transmission of HIV
Virus Assembly as a Target for Antiretroviral Therapy.Digital Access Springer 2013 - ArticleDavis P, Percy JS.Br J Dermatol. 1978 Aug;99(2):201-5.In vivo and in vitro animal experiments have been performed to clarify the role of ultraviolet light denatured DNA (UV DNA) and ultraviolet light (UVL) in the pathogenesis of the dermal lesions of human SLE. Rabbits immunized with UV DNA show deposition of immunoglobulin at the dermal-epidermal junction following exposure to UVL. We have also shown that UV DNA appears concomitantly with the antibody at the dermal-epidermal junction subsequent to the UVL exposure. Both n DNA and UV DNA have been shown to bind to the dermal-epidermal junction in vitro which could result in the persistence of these antigens at this site. These studies lend further support to the hypothesis that the release of UV DNA and its subsequent deposition at the dermal-epidermal junction may result in binding of both immunoglobulin and complement, leading to the development of histological lesions of SLE.