Pathology
Once the virus has entered the host cells, the viral genome is transcribed and integrated with the host DNA and begins replicating many times, as described above. During this stage, the person is still asymptomatic. The presence of antibodies in the blood, known as seroconversion, takes place in the first 3-6 weeks of the replication process.
Further infection is achieved when the virus and viral-infected cells reach the lymph nodes, where activated CD4+CCR5+ T cells are targeted by the virus. Thus, the immune system’s response actually spreads the virus by presenting it to additional immune cells (T-cells) that can be further infected; resulting in the massive depletion of CD4+ memory T cells. The CD4 count is a way to track the progress of the HIV infection; at this stage the CD4 count is still above 500 cells/mm3.
After 21-28 days, the virus enters the blood again to infect the remaining lymphocytes resulting in peak plasma viraemia along with decreased numbers of peripheral CD4+ T cells. During this peak viral load, the virus now becomes clinically apparent (flu-like symptoms) as the CD4 count has decreased to 200-500 cells/mm3.
Following the acute phase, the immune system responds strongly in order to decrease the viral load and increase the circulating CD4+ T cells; however, despite this attempt the host is not able to clear the infection. Over 12-20 weeks, the viral load eventually decreases which begins a more chronic stage of infection. Although circulating CD4+ T cells return to a near normal level, studies have found accelerated cell turnover and massive activation of the immune system during this chronic HIV infection. When an individuals’ CD4 (T cell) count is below 200 cells/mm3, it is known as acquired immunodeficiency syndrome (AIDS)
Pathology Once the virus has entered the host cells, the viral genome is transcribed and integrated with the host DNA and begins replicating many times, as described above. During this stage, the person is still asymptomatic. The presence of antibodies in the blood, known as seroconversion, takes place in the first 3-6 weeks of the replication process. Further infection is achieved when the virus and viral-infected cells reach the lymph nodes, where activated CD4+CCR5+ T cells are targeted by the virus. Thus, the immune system’s response actually spreads the virus by presenting it to additional immune cells (T-cells) that can be further infected; resulting in the massive depletion of CD4+ memory T cells. The CD4 count is a way to track the progress of the HIV infection; at this stage the CD4 count is still above 500 cells/mm3. After 21-28 days, the virus enters the blood again to infect the remaining lymphocytes resulting in peak plasma viraemia along with decreased numbers of peripheral CD4+ T cells. During this peak viral load, the virus now becomes clinically apparent (flu-like symptoms) as the CD4 count has decreased to 200-500 cells/mm3. Following the acute phase, the immune system responds strongly in order to decrease the viral load and increase the circulating CD4+ T cells; however, despite this attempt the host is not able to clear the infection. Over 12-20 weeks, the viral load eventually decreases which begins a more chronic stage of infection. Although circulating CD4+ T cells return to a near normal level, studies have found accelerated cell turnover and massive activation of the immune system during this chronic HIV infection. When an individuals’ CD4 (T cell) count is below 200 cells/mm3, it is known as acquired immunodeficiency syndrome (AIDS)
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