It kills of the virus while strengthening the immune system
ss and yes
But I could be wrong so sorry if I am.
Answer:
Give at least 3 reasons why viruses are considered non-living and therefore NOT classified into the Linnaean system of life.
Viruses as we know that they are micro-organism but they are not produced from cell
Viruses does not grow rather undergo replication by multiplying into several number within minutes
also they rely on host energy as they could not produce energy needed for their usage.
Explanation:
Every living organism are made up of cells which makes it the fundamental unit of life where virus does not fall into such category, Growth is an essential characteristics of every living organisms, viruses only replicate rather they does not undergo growth.
Given what we know, we can confirm that the "balance of nature" refers to a scientific theory about ecological homeostasis.
<h3>What does ecological homeostasis mean?</h3>
- This refers to the idea of a perfect balance in an ecosystem.
- It is the theory that all aspects of an ecosystem are and will remain balanced even if there are small changes.
- This implies that any minor change in an ecosystem will be corrected.
- This will happen through natural regulation mechanisms such as positive or negative feedback.
Therefore, we can confirm that the "balance of nature" is the scientific theory that all things in an ecosystem will remain balanced, meaning that if there is a small change, it will be corrected through some form of natural regulatory mechanism.
To learn more about ecosystems visit:
brainly.com/question/1673533?referrer=searchResults
<span>he Streptococcus pneumoniae capsule is vital for virulence and may inhibit complement activity and phagocytosis. However, there are only limited data on the mechanisms by which the capsule affects complement and the consequences for S. pneumoniae interactions with phagocytes. Using unencapsulated serotype 2 and 4 S. pneumoniae mutants, we have confirmed that the capsule has several effects on complement activity. The capsule impaired bacterial opsonization with C3b/iC3b by both the alternative and classical complement pathways and also inhibited conversion of C3b bound to the bacterial surface to iC3b. There was increased binding of the classical pathway mediators immunoglobulin G (IgG) and C-reactive protein (CRP) to unencapsulated S. pneumoniae, indicating that the capsule could inhibit classical pathway complement activity by masking antibody recognition of subcapsular antigens, as well as by inhibiting CRP binding. Cleavage of serum IgG by the enzyme IdeS reduced C3b/iC3b deposition on all of the strains, but there were still marked increases in C3b/iC3b deposition on unencapsulated TIGR4 and D39 strains compared to encapsulated strains, suggesting that the capsule inhibits both IgG-mediated and IgG-independent complement activity against S. pneumoniae. Unencapsulated strains were more susceptible to neutrophil phagocytosis after incubation in normal serum, normal serum treated with IdeS, complement-deficient serum, and complement-deficient serum treated with IdeS or in buffer alone, suggesting that the capsule inhibits phagocytosis mediated by FcÎł receptors, complement receptors, and nonopsonic receptors. Overall, these data show that the S. pneumoniae capsule affects multiple aspects of complement- and neutrophil-mediated immunity, resulting in a profound inhibition of opsonophagocytosis.</span>
