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15/6 Thesis defense by Jamirah Nazziwa

Jamirah Nazziwa will defend her thesis: Dynamics of HIV-1 infection within and between hosts.

Date: 2022-06-15
Time: 13:00
Place: Agardh lecture hall, CRC, Jan Waldenströms gata 35, Malmö or
you can join by Zoom,
Professor Fernando Gonzalez Candelas,
University of Valencia, Spain 

Dynamics of HIV-1 infection within and between hosts-Lund University.

Popular summary
HIV-1 is one of the deadliest viruses in human history, having killed between 27 and 48 million individuals since the epidemic began in the 1980s. By the end of 2020, around 38 million people were living with AIDS, with approximately 73% receiving antiretroviral medication. Despite treatment expansion, 1.5 million people were newly infected with HIV-1 and 680,000 were diagnosed with AIDS-related illnesses, with children accounting for 15% of the total. HIV-1 transmissions are most common in the initial few weeks following infection, when the virus load in the blood is highest and most persons are ignorant of their serostatus. Because HIV-1 attacks and slowly destroys immune system cells, and it constantly mutates to weaken or conceal from these cells' action, HIV-1 can be present for three to ten years before an infected individual develops AIDS if not treated. We were able to investigate when the virus was introduced and how it propagated within Nigeria by looking at how HIV-1 has evolved in Nigeria, the country with the highest number of AIDS-related deaths in the world. We found three main forms of HIV-1 circulating in Nigeria: CRF02_AG, CRF43_02G, and subtype D, which were introduced as five significant sub-epidemics in the 1960s and 1970s. According to HIV-1 migration analysis, HIV-1 first emerged and spread in urban areas such as Abuja and Lagos before spreading to smaller communities. A systematic review of other studies on the topic revealed similar movement patterns in other Western African countries, with cross-border transmissions; nevertheless, certain epidemics in Eastern and Southern Africa are localised, with little indication of mixing with surrounding populations. We were able to explore why some people experience symptoms during the first two weeks after infection while others do not by looking at how individuals responded to early innate immune responses in the first two weeks after infection. We discovered that those who have a stronger innate immune response are more likely to experience acute infection symptoms than those who have a lesser response. IP-10, for example, is 14 times greater and independently associated with these symptoms, and can be utilised to identify people with stronger immune responses. We also discovered that each 18 individual has a specific protein expression profile and that 21 per cent of the plasma proteome significantly changed before and during the first month of acute HIV-1 infection. Among the top proteins are vWF, FGN1, and GRN1, which have roles in immune activation and disease. We also identified proteins that differed considerably between individuals who progressed slowly and quickly, as well as those who had or did not have acute retroviral syndrome. We attempted to discover the mechanisms by which the virus interacts with the host during acute infection and how they interact to control the rate of disease progression. Finally, we investigated how the virus evolves within an infant during his or her first year of life. Within an untreated individual, HIV-1 generates roughly a billion virus particles every two-three days, but only one or a handful of these virus variants are transmitted from the donor to the recipient. To understand the dynamics of these transmitted viruses, studies of these transmitted variants have mostly been conducted in adults. When we studied the HIV-1 transmission dynamics in infants, we discovered that the infection was caused by a single variant in 78 per cent of the infants, infection was caused by a single variant transmitted from the mother. The virus began to escape from the action of immune cells at three months, and the mutations responsible for this escape were transmitted from the mother and remained throughout the first year. Furthermore, viruses with escape mutations evolved faster than those without. This work sheds light on how the infant immune selection pressure influences how HIV-1 evolves within infants.