TB targets your brothers friends uncles sons cows foot.
No, Mycobacterium tuberculosis does not produce exotoxins. It mainly causes disease through its cell wall components and induces an inflammatory response in the host.
Antiviral medications are designed to target specific proteins or enzymes unique to the virus, which are not found in host cells. This selectivity allows the medication to inhibit viral replication without harming the host cell. Additionally, antiviral medications are often metabolized or eliminated from the body before they can affect host cells.
No, drug-susceptible cells and drug-resistant cells are equally likely to infect a new host.
A virus attaches to a host cell by recognizing and binding to specific proteins or receptors on the cell surface. This attachment is necessary for the virus to enter the host cell and begin the process of infection.
The specific viral proteins on the surface of the virus determine its attachment to host cell membrane receptors. These proteins bind to complementary host cell receptors, allowing the virus to attach and enter the host cell.
Viruses do not have a habitat in the traditional sense, as they are not considered living organisms. They require a host cell to replicate and survive. Once inside a host, viruses can exist in various parts of the body, depending on the type of virus and its specific target cells.
One common method a virus uses to inject itself into its target is through receptor-mediated endocytosis. In this process, the virus binds to specific receptors on the surface of the host cell, triggering the cell to engulf the virus in a membrane-bound vesicle. Once inside, the virus can release its genetic material into the host cell's cytoplasm, allowing it to hijack the cell's machinery for replication. Other methods include direct fusion with the cell membrane or utilizing specialized structures like viral injectisomes.
Yes, the mumps virus attaches to the surface of the host cell through specific interactions between its hemagglutinin-neuraminidase (HN) protein and sialic acid receptors on the host cell membrane. This attachment is a crucial first step for the virus to enter the host cell and initiate infection. Once attached, the virus can then fuse with the host cell membrane, allowing it to release its genetic material into the host cell.
Yes, preventing the specific attachment of a virus to its host cells can be an effective way to prevent infection. By blocking the receptors on the host cell that the virus recognizes for attachment, the virus is unable to enter the cell and replicate, thus reducing the likelihood of infection. This can be achieved through various means, such as developing drugs or vaccines that target the attachment process.
Mycobacterium tuberculosis, the bacterium that causes tuberculosis, primarily relies on the host's cellular environment for nutrients. It absorbs fatty acids, amino acids, and other organic compounds present in the host's tissues and cells. Unlike many bacteria, it has a unique cell wall structure that allows it to survive in harsh conditions and utilize a limited range of nutrients. Its metabolic processes are adapted to thrive within the macrophages of the immune system.
The base plate of a virus, particularly in bacteriophages, plays a crucial role in the infection process. It serves as a structural component that anchors the virus to the host cell membrane, facilitating the delivery of the viral genome into the host. Additionally, the base plate may contain proteins that help recognize and bind to specific receptors on the host cell, ensuring a successful infection. Overall, it acts as a vital interface between the virus and its target host.
Mycobacterium tuberculosis, the bacterium causing tuberculosis, has a unique cell wall structure characterized by a thick layer of mycolic acids and peptidoglycan, which contributes to its acid-fastness. This structure protects the bacterium from desiccation and immune responses, allowing it to survive in harsh environments. Additionally, the presence of complex lipids in its cell wall can trigger strong inflammatory responses, leading to tissue damage in the host and the formation of granulomas, which are hallmark features of tuberculosis infections.