Human immunodeficiency virus (HIV) preferentially destroys CD4+ cells. Specifically, what effect does this have on antibody and cell-mediated immunity?
For your additional reference, I have included two videos for you to watch.
The first video reviews HIV and its replication cycle of HIV as well as how it targets T-helper cells. https://www.youtube.com/watch?v=ng22Ucr33aw
I have also attached a powerpoint on HIV that covers key facts regarding the virus.
The second video is on the adaptive immune response and the functions of T cells. https://www.youtube.com/watch?v=6DxcrObJJRg
After you watch the videos and complete your readings, use your knowledge to address this weeks prompts.
This week we are shifting our focus to the infectious disease process and all the various factors that are needed for pathogenesis to begin as well as to looking at the functions of the innate and adaptive immune system responses and how our body uses these responses to protect us against pathogenic agents. Learning about the ways by which our immune system works against infectious microbes also helps us to understand how microorganisms utilize their virulence factors to work against host immune system surveillance and immunological responses. Our discussion forum this week will look at the impact that the human immunodeficiency virus (HIV) has on our cell-mediated immunity. HIV is an enveloped, positive-sense, single-stranded RNA virus that is also a retrovirus (think back to what you learned about retroviruses in Chapter 13 a few weeks ago). As an enveloped virus it has glycoprotein spikes that it uses to recognize and attach to and infect T-helper cells within our immune system. As you will learn from Chapter 16, these cells Helper T cells are one of the most important cells in our adaptive immune response. Among their many functions are the activation of B cells to secrete antibodies, the activation of macrophages to destroy ingested microbes, and the activation of cytotoxic T cells to kill infected target cells (Alberts et. Al., 2002).
