Measles pathogenesis curve by function #f# (see details for questions)?

Question

This question is relevant to Area Between Curves.

I don't know what that constitutes under Socratic guidelines, so it is mentioned here.

A patient infected with the measles virus who has some immunity to the virus has a pathogenesis curve that can be modeled by, for instance, #g(t)=0.9f(t).#

If the threshold concentration of the virus required for infectiousness to begin is #"1210 cells/mL"#, on what day does this occur?

Let #P_3# be the point on the graph of #g# where infectiousness begins. It has been shown that infectiousness ends at a point #P_4# on the graph of #g# where the line through #P_3#, #P_4# has the slope #-23#. On what day does infectiousness end?

Compute the level of infectiousness for this patient.

Scarlett Allison · Accepted Answer

Hi...this is only an attempt, completely without any (probable) connection with your question....because I didn't know the function #f(t)# so I tried with something I found on the internet!!!

I found on the internet this:
https://tutor.hix.ai

Scarlett Allison · Answer

undefined The pathogenesis of measles follows a typical pattern characterized by several distinct stages.

1. Incubation Period: Typically lasts for 10-14 days after exposure to the measles virus. During this time, the virus begins to replicate within the respiratory tract and spreads to regional lymph nodes.

2. Prodromal Stage: Lasts for 2-4 days and is characterized by nonspecific symptoms such as fever, malaise, cough, coryza (runny nose), and conjunctivitis (red eyes). The characteristic Koplik spots may also appear on the buccal mucosa.

3. Exanthematous Stage: This stage marks the appearance of the characteristic measles rash, which typically begins on the face and spreads downwards to involve the trunk and extremities over a period of 3-4 days. The rash is erythematous and maculopapular in nature.

4. Recovery: Following the resolution of the rash, most individuals recover from measles. However, complications such as pneumonia, otitis media, encephalitis, or subacute sclerosing panencephalitis (SSPE) may occur, particularly in immunocompromised individuals or those with vitamin A deficiency.

The pathogenesis of measles is primarily mediated by the virus's ability to infect and replicate within immune cells, leading to widespread systemic dissemination and immune dysregulation. Additionally, the virus can cause direct cytopathic effects on infected cells, contributing to tissue damage and clinical manifestations. The host's immune response, particularly cell-mediated immunity, plays a crucial role in controlling viral replication and resolving the infection. However, excessive or dysregulated immune responses can also contribute to tissue damage and the development of complications associated with measles.