That would fit the mathematical model nicely. Notice that I did not specify the mechanism for increased growth; I only postulated that there was some genetic makeup that would enable it. Perhaps it is this gene. Moreover, if this gene is specific to the growth rate / virility, then other aspects of the genetic makeup could vary without affecting the growth. That would also fit well with the broad genetic optimum assumption in the model.
This is one of the things that appears to have the epidemiologists on edge.
Clearly.
Now I know that this outbreak is Marburg but, as Kelly_2000 pointed out to redoglum in post 1217, in part, "...it is Marburg and something entirely new." .....
Since the first signs of the outbreak occurred in October 2004 how many cases infected others before knowing it was Marburg? This is, essentially, a rhetorical question. However, if I understand your modeling correctly it appears to fit your modeling represented by Figure D.
Second point first. Excellent point and I think the data support this. Indeed, my earlier plots showed this explicitly. Namely, the epidemiological growth was faster in the earlier stages of the epidemic. When the virus was identified, better isolation was instituted. I have not modelled the data that way this last time because there are too many unknowns.
The issue of classification of the virus, i.e. : Marburg, a variant of Marburg, Ebola, Angola Hemorrhagic Fever, etc. is largely a moot point IMHO. I believe there is no significant difference. The classification serves no purpose in understanding or modelling; it is merely taxonomy.
Now, taxonomy generally has a purpose, largely to break up complicated problems into simpler ones. However, it can be overdone and become restrictive, and I believe that is the case here. We are arguing about the name of the thing. Call it an umtyfratz if you want. It doesn't change the underlying dynamics.
There appears to be no structural, essential difference between any of these viral variants. They are all filovirii (i.e. their structure is filamentary). They all consist of an amino acid sheath surrounding an RNA core. They all work the same way. They all are hemorrhagic fevers. The genetic makeup is about the same length and complexity.
Clearly, the exact genetic makeup differs. However, it can equally accurately be viewed as a single virus type, such that there are specific genetic combinations that provide successful growth. My original model postulated a growth function that was a single peak: it was a Gaussian. However, by contrast, imagine a growth function with several peaks (and valleys). The peaks correspond to the different names of the disease (e.g. Ebola, Marburg, etc.). The valleys correspond to nothing; they die out. Some of the peaks are higher and broader than others. However, essentially, this is all the same virus with modest genetic changes. What is significant is that this particular genetic combination of this virus may have a faster growth rate and a broader distribution than others. Name it anything you please.