Lecture 5 flashcards

Introduction to Viruses and Immune Response

The session begins with informal greetings and mentions of coffee, creating a relaxed atmosphere that encourages open discussion about viruses, specifically focusing on SARS-CoV-2 and the complex immune responses elicited by infections. The instructor aims to build upon the foundational knowledge gained from the previous semester regarding infectious agents and the intricacies of the immune system. Emphasizing the significance of understanding viral behavior, the discussion highlights how viruses effectively evade immune responses to establish infection and persist in the host.

Overview of Viral Invasion and Immune Evasion

The lecture centers on the intricate structure and life cycle of viruses, starting from the fundamental processes of viral attachment to host receptors, through invasion, and subsequent replication.

Key Stages of the Viral Life Cycle:

• Attachment to Host Cell Receptors:The initial step in the viral life cycle involves specific viral proteins, such as the spike protein in the case of SARS-CoV-2, binding to corresponding receptors (ACE2) on the host cell surface. This binding is crucial for facilitating the virus's entry into the host cell.

• Entry of Viral RNA:Following attachment, the viral RNA is injected into the host cell where it hijacks the cellular machinery, instructing the host to replicate its genetic material. This replication results in the production of numerous copies of the virus, often at a rapid pace.

• Assembly and Release:Newly synthesized viral particles are assembled within the host cell and subsequently released to infect neighboring cells. The efficiency of this replication process significantly contributes to the virus’s ability to spread throughout the host organism.

• RNA Manipulation:Viruses exhibit a sophisticated capacity to alter their RNA sequences to evade detection by the host's immune system. This adaptive mechanism is vital for their continued virulence and is a central theme elaborated upon throughout the lecture.

Role of Toll-like Receptors (TLRs)

Toll-like receptors (TLRs) are pivotal in the immune system's ability to identify viral infections. Each virus possesses unique nucleic acid profiles, such as RNA for SARS-CoV-2 and DNA for herpes and smallpox, which activate distinct immune response pathways.

For instance, TLRs recognize viral RNA and trigger signaling cascades to activate immune cells, enhancing the body's defense against the infection. SARS-CoV-2 employs sophisticated strategies to modify its RNA structure, allowing it to remain concealed from immune recognition, which significantly impacts its replication and survival.

Immune System Response

Once the virus is detected, the immune system engages through various mechanisms:

• Recognition via MHC Molecules:Infected cells are identified by major histocompatibility complex (MHC) class I molecules, which present viral peptides to cytotoxic T-cells, triggering cell-mediated immunity essential for clearing the infection.

• Activation of Cytotoxic T-cells:These immune cells proliferate in response to infection and are key to eliminating virus-infected cells, showcasing the importance of a robust T-cell response.

• Role of Antibodies:Effective immune responses often hinge on generating neutralizing antibodies that block viral entry by preventing binding to ACE2 receptors, specifically emphasizing the critical role of antibodies in response to SARS-CoV-2.

Challenges in Immune Response

Despite the immune system's robust mechanisms, responses can be delayed due to the rapid replication of viruses and their cunning evasion tactics.

• Limitations of Non-Specific Antibodies:Often, non-specific antibodies do not provide adequate protection against viral infections, highlighting the need for the adaptive immune system to produce specific, high-affinity antibodies tailored to the virus.

• Persistent Infections:Certain viruses, such as herpes and Epstein-Barr virus, can maintain a dormant status within the body, creating challenges for immune surveillance and leading to potential reactivation and associated diseases.

Specific Viruses and Their Mechanisms

• HIV (Human Immunodeficiency Virus):A retrovirus that specifically targets CD4 T-cells, leading to progressive immune dysfunction. Its ability to integrate into the host genome complicates immune detection, making treatment and management challenging.

• Epstein-Barr Virus (EBV):Primarily targets B-cells, establishing lifelong infections that may result in various diseases, including malignancies and other reactivation-related pathologies.

The Importance of Antiretroviral Therapy (ART)

The discussion explores how ART effectively targets multiple stages of HIV replication, achieving reduced viral loads to undetectable levels. This reduction is crucial for preserving immune function and overall health. The session also examines future therapeutic avenues such as genetic and stem cell therapies that hold the potential to achieve functional cures by targeting viral reservoirs in the body.

Clinical Implications and Research Advances

A strong emphasis is placed on how understanding the immune evasion strategies of viruses like SARS-CoV-2 can directly inform vaccine development and therapeutic strategies, shaping public health approaches to pandemics. Furthermore, discussions on the implications of intensive farming practices and zoonotic disease transmission underscore the interconnections between human activities and the emergence of viral outbreaks, highlighting emerging risks associated with global health.

Concluding Thoughts

The session concludes by reaffirming the importance of ongoing engagement with scientific literature and research methodologies, empowering students in their future academic and professional undertakings in the biological sciences. The instructor encourages an interactive environment, fostering questions and participation in unpacking the complex topics surrounding viral immunity and epidemiology, emphasizing their crucial role in addressing current global health challenges.