Answer:
The difference between both infections is that viral infections where the virus is latent, this virus once infected is protected in the nerves of the animal organism, as for example in humans the herpes family viruses (HSV1) are housed in ganglionic terminals such as the trigeminal ganglion or the V cranial nerve, so that in a situation of immunodepression, reinfect the individual again, causing him to be unable to remove the virus from his body.
On the other hand, persistent infections diseases are the threats that persist because the microorganism cannot be eliminated, either because it is very complex, or the cure does not exist, or the correct treatment is not carried out. Furthermore, it is necessary to consider that some microorganisms mutate becoming resistant to these drugs and thus persist longer in the body until they are eliminated.
Explanation:
In short, latency refers to the fact that the individual lives with the virus for life, and persistence is that it is possible to eliminate it over a long period of time since the infectious microorganism is considered very difficult.
Answer:
it A
Explanation:
pick A hopefully it right
Answer:
One of the common genetic disorders is sickle cell anemia, in which 2 recessive alleles must meet to allow for destruction and alteration in the morphology of red blood cells. This usually leads to loss of proper binding of oxygen to hemoglobin and curved, sickle-shaped erythrocytes. The mutation causing this disease occurs in the 6th codon of the HBB gene encoding the hemoglobin subunit β (β-globin), a protein, serving as an integral part of the adult hemoglobin A (HbA), which is a heterotetramer of 2 α chains and 2 β chains that is responsible for binding to the oxygen in the blood. This mutation changes a charged glutamic acid to a hydrophobic valine residue and disrupts the tertiary structure and stability of the hemoglobin molecule. Since in the field of protein intrinsic disorder, charged and polar residues are typically considered as disorder promoting, in opposite to the order-promoting non-polar hydrophobic residues, in this study we attempted to answer a question if intrinsic disorder might have a role in the pathogenesis of sickle cell anemia. To this end, several disorder predictors were utilized to evaluate the presence of intrinsically disordered regions in all subunits of human hemoglobin: α, β, δ, ε, ζ, γ1, and γ2. Then, structural analysis was completed by using the SWISS-MODEL Repository to visualize the outputs of the disorder predictors. Finally, Uniprot STRING and D2P2 were used to determine biochemical interactome and protein partners for each hemoglobin subunit along with analyzing their posttranslational modifications. All these properties were used to determine any differences between the 6 different types of subunits of hemoglobin and to correlate the mutation leading to sickle cell anemia with intrinsic disorder propensity.
Explanation:
