Hiv Infection Model
Hiv Infection Model - Related Videos
03:13
Establishing an Active HIV Infection in a Rat Model
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2025
This video demonstrates the procedure of injecting chimeric HIV viruses into the cortex of a rat's brain, where the virus RNA integrates into the host genome, replicates, and spreads to establish an active HIV infection in the experimental model.
02:49
Generation of an In Vitro Cell Culture Model of Malaria-HIV Co-Infection
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2025
This video demonstrates the generation of an in vitro malaria-HIV co-infection cell culture model. HIV-infected peripheral blood mononuclear cells co-cultured with Plasmodium falciparum parasitized erythrocytes potentially support each other's growth and provide insights into the immune responses and disease progression in HIV and malaria co-infections.
08:14
An In Vitro Model for Measuring Immune Responses to Malaria in the Context of HIV Co-infection
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Cited by 1 •
2015
Human co-infection is difficult to replicate in vitro. However, human malaria parasites can readily be cultured in vitro, as can freshly isolated human peripheral blood mononuclear cells naturally infected with HIV. This provides an excellent model for studying early immune responses to malaria parasites in the context of HIV co-infection.
04:51
A Human Cervical Mucosa Infection Model to Study HIV Pathogenesis in Ex Vivo Conditions
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2025
This video demonstrates ex vivo infection of human uterine mucosal tissue with human immunodeficiency virus type 1, HIV-1, and their maintenance on top of gelatin sponges at the air-liquid interface. This method allows monitoring of HIV-1 replication and pathogenesis within human tissues.
11:38
Stem-cell Based Engineered Immunity Against HIV Infection in the Humanized Mouse Model
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Cited by 19 •
2016
This protocol describes the methods in constructing a humanized bone-marrow/liver/thymus mouse model with stem cell-based engineered immunity against HIV infection.
FAQs
Receptor availability determines which cells can support viral entry. HIV first engages CD4 and then uses CCR5 or CXCR4 as a co-receptor, after which reverse transcription converts viral information into a DNA form that can integrate into the host genome. Comparing models with different susceptible cell populations helps investigators examine infection patterns and their consequences for neural systems.
Inflammatory signaling provides a mechanism linking infection in immune or glial cells to impaired neural function, even when neurons are not the primary infected population. HIV infection models allow researchers to examine interactions among these cell types and determine how inflammatory responses contribute to HIV-associated neurocognitive disorders within cellular, organoid, or organism-level systems.
Cell cultures, brain organoids, and animal models provide complementary levels of biological organization. Cultures support controlled examination of susceptible cells and cellular responses, organoids provide a three-dimensional neural context, and animal models extend investigation to interactions within an organism. Together, these systems help connect viral processes with tissue-level consequences and broader neurological outcomes.
These models can be used to examine how antiretroviral treatment affects HIV-related processes and their neural consequences. Applying treatment within a controlled experimental system allows investigators to compare infection or inflammatory effects with treated conditions. This is particularly relevant when studying whether treatment alters mechanisms associated with neurocognitive impairment or helps identify remaining targets for neuroprotective intervention.
Model selection depends on the biological question being tested. Cell cultures are appropriate for focused studies of infection, susceptible cells, or inflammatory signaling, whereas brain organoids and animal models support investigation of more complex neural interactions. Using multiple model types can strengthen interpretation by relating controlled cellular findings to tissue or organism-level effects.
They can reveal how viral infection, immune or glial-cell interactions, and inflammatory signaling relate to impaired neural function. In neuroscience, these outcomes help clarify mechanisms associated with HIV-associated neurocognitive disorders and provide systems for evaluating potential neuroprotective interventions. The models also support comparison of disease-related effects with changes observed during antiretroviral treatment.