Question

You discover a mouse immune to infection by a certain type of retrovirus normally pathogenic towards that strain. Further study reveals that the retrovirus does not enter the cells of this mouse. What is the most likely explanation for your observation? Would you expect other retroviruses of the same interference group to be able to infect this mouse? Why or why not?

Short answer

The likely explanation for the mouse's immunity to the retrovirus infection is a genetic mutation, which resulted in a change or absence of the specific cell surface receptor that the retrovirus binds to. Without this receptor, the retrovirus cannot enter or infect the cell. Considering retroviruses of the same interference group - a group of viruses that target the same receptor - they would also likely be unable to infect this mouse. This is because, if the targeted receptor is altered or missing, then these retroviruses would also be unable to enter the mouse's cells.

Step-by-step solution

Understanding how retroviruses enter cells

Retroviruses enter cells by binding to specific cell surface receptors. Once the binding occurs, the virus fuses with the cell membrane, enabling it to enter the cell and replicate its genetic material.

Consider possible explanations for the observed immunity

The most likely explanation for the observation in this exercise is that the mouse has a genetic mutation, resulting in either the absence or alteration of the cell surface receptor that the retrovirus usually binds to. Without the proper receptor, the retrovirus cannot enter the cell and cause an infection.

Understanding interference groups

An interference group is a group of viruses that share the same cell surface receptor for entry into cells. Viruses in the same interference group compete for binding to the same receptor, and a cell infected by one virus may be resistant to infection by other viruses in the same interference group.

Determine the likelihood of infection by other retroviruses

Given that the mouse is immune to infection by the particular retrovirus due to likely absence or alteration of the cell surface receptor, it would be expected that other retroviruses from the same interference group would also be unable to infect the mouse. This is because they would also be targeting the same receptor, which is either absent or altered, and therefore not functional in allowing entry of retroviruses.

Conclusion

In summary, the most likely explanation for the observation that this mouse is immune to infection by a certain type of retrovirus is the genetic mutation leading to an absent or altered cell surface receptor, preventing the particular retrovirus from entering its cells. It is expected that other retroviruses from the same interference group would also be unable to infect this mouse, as they would target the same receptor which is not functional in this case.

Key concepts

Cell Surface Receptors and Viral Entry

To understand why certain mice might exhibit immunity to specific retroviruses, one must first grasp the role of cell surface receptors in viral infections. Retroviruses, like many other viruses, gain entry into a host cell by latching onto specific proteins on the cell's exterior called cell surface receptors. These receptors serve as gatekeepers and are crucial for normal cell function, including communication and regulation of cell-to-cell interactions.

During a normal infection cycle, a retrovirus recognizes and binds to its corresponding receptor through a 'lock and key' mechanism. This binding triggers the fusion of the viral envelope with the cell membrane, allowing the viral genetic material to enter and hijack the cell's machinery for its replication. If a receptor is missing or altered due to a mutation, as suggested in the exercise, the virus cannot bind effectively, and thus, the entry and subsequent infection are impeded.

In the scenario described, the resistant mouse likely has a modification in the cell surface receptor that the retrovirus normally targets. This small genetic change can have a profound impact, rendering the virus unable to recognize its entry point, much like a key failing to fit a changed lock. Consequently, understanding these receptors is pivotal for developing therapies and preventive measures against viral diseases.

The Role of Genetic Mutation in Immunity

Genetic mutations are inheritable changes in the DNA sequence that can lead to variations in the physical characteristics or abilities of an organism. These changes sometimes provide an evolutionary advantage, such as resistance to certain diseases. The exercise highlights a mouse with a mutation that confers immunity to a retrovirus; this mutation likely affects the structure or expression of a cell surface receptor.

There are various types of mutations, ranging from single nucleotide polymorphisms, where a single basepair is altered, to larger deletions or insertions. A mutation affecting the viral entry process could result from subtle changes in the receptor's amino acid sequence, leading to structural rearrangements that prevent viral recognition or binding. Alternatively, a mutation could completely knock out the receptor's expression, leaving the virus with no anchor point on the cell surface.

Understanding genetic mutations provides a window into the mechanisms of resistance and can guide the development of genetic screenings or novel treatments. In vaccine development, for example, knowing which mutations confer resistance can help design strategies that mimic these alterations to induce immunity in the wider population.

Viral Interference Group Mechanics

The concept of a 'viral interference group' is fundamental when considering why the mouse in the exercise would be resistant not only to one retrovirus but potentially others as well. These groups are classified based on the shared reliance on a specific cell surface receptor for entry into a host cell. Retroviruses within the same interference group are in direct competition for the same 'lock' - that is, the receptor they need to 'unlock' to infect a cell.

If a host cell is infected by one retrovirus from the group, it can often become resistant to superinfection by other members of the group - a phenomenon known as 'viral interference'. Additionally, as seen in the immune mouse, a genetic mutation rendering the receptor nonfunctional will confer resistance to all retroviruses within that interference group, since none can bind effectively.

Viral interference has medical implications. Understanding the dynamics within these groups can lead to novel antiviral strategies, such as the engineering of benign viruses that compete for cell receptors, thereby protecting against more pathogenic strains. Thus, the study of viral interference is not only academic but also a potential pathway to innovative treatments and prevention measures in the ongoing battle against viral infections.