Search results
Results from the WOW.Com Content Network
Cyanobacteria (blue-green algae) bloom on Lake Erie (United States) in 2009. These kinds of algae can cause harmful algal bloom. A harmful algal bloom (HAB), or excessive algae growth, is an algal bloom that causes negative impacts to other organisms by production of natural algae-produced toxins, water deoxygenation, mechanical damage to other organisms, or by other means.
Microsporidia are restricted to animal hosts, and all major groups of animals host microsporidia. Most infect insects , but they are also responsible for common diseases of crustaceans and fish . The named species of microsporidia usually infect one host species or a group of closely related taxa.
This type of cell death is called "accidental cell death" (ACD). "Regulated cell death (RCD)" is encoded by a genetic pathway that can be modulated by genetic or pharmacologic interventions. Programmed cell death (PCD) is a type of RCD that occurs as a developmental program, and has not been addressed in cyanobacteria yet.
The reticulate bodies must use some of the host's cellular machinery to complete their replication. The reticulate bodies then convert back to elementary bodies, and are released back into the lung, often after causing the death of the host cell. The EBs are thereafter able to infect new cells, either in the same organism or in a new host.
The rickettsiae use the actin to propel themselves throughout the cytosol to the surface of the host cell. This causes the host cell membrane to protrude outward and invaginate the membrane of an adjacent cell. [21] The bacteria are then taken up by the neighboring cell in a double membrane vacuole that the bacteria can subsequently lyse ...
When the extracellular phase (EB) infects the host eukaryotic cell via endocytosis the bacteria transforms into the replicative phase (RB) while remaining in a membrane-bound vesicle called an inclusion. [6] Within the inclusion the RB cells will avoid the host cell's defenses, such as lysosomes, grow, and divide by binary fission. [6]
Cell receptor ephrin-B2, which is located on epithelial cells around smaller arteries, neurons, and smooth muscle cells, is targeted by the viral protein G. [25] Once the protein G binds to ephrin-B2, the viral protein F facilitates fusion with the host cell membrane and releases viral RNA into the host cell cytoplasm. [26]
The herpes virus can then exit this dormant stage and re-enter the lytic cycle, causing disease symptoms. Thus, while herpes viruses can enter both the lytic and lysogenic cycles, latency allows the virus to survive and evade detection by the immune system due to low viral gene expression. The model organism for studying lysogeny is the lambda ...