This document summarizes research on the differences in spread patterns between respiratory viruses like COVID-19, SARS, and influenza compared to smallpox. It analyzes how virus size may influence transmission methods, with smaller viruses like coronaviruses being more capable of airborne spread over longer distances than larger viruses like smallpox. Maps and figures are presented showing the diffusion of historical outbreaks like the 1918 Spanish flu, 1968 Hong Kong flu, and 18th century smallpox epidemics in North America to illustrate variations in timing, velocity, and distance of spread. The authors conclude that airborne transmission over longer ranges helps explain the rapid increase in COVID-19 cases seen in some areas compared to the more localized patterns of small

1. BOOK
Title : RESPIRATORY VIRUS PATTERN OF DIFFUSION : SIZE
INFLUENCE
Authors:
1) Luisetto m IMA ACADEMY Marijnskaja NATURAL SCIENCE
BRANCH itlay 29121
2) Naseer Almukthar, Professor, Department of Physiology /College
of Medicine, University of Babylon, Iraq
3) Prof. Giulio Tarro Primario emerito dell’ Azienda Ospedaliera “D.
Cotugno”,Napoli
Chairman della Commissione sulle Biotecnologie della Virosfera,
WABT -
UNESCO, Parigi, Rector of the University Thomas More U.P.T.M.,
Rome
Presidente della Fondazione de Beaumont Bonelli per le ricerche
sul cancro -ONLUS, Napoli
4)Behzad Nili Ahmadabadi, Innovative Pharmaceutical product
development specialist, USA
5)Ahmed Yesvi Rafa , Founder and President, Yugen Research
Organization; Undergraduate Student, Western Michigan University,
MI, USA 49008
6)Ghulam Rasool Mashori Department of Medical & Health Sciences
for Woman, Peoples University of Medical and Health Sciences for
Women,Pakistan
7)Tuweh Prince GADAMA the great, Professor,Cypress University
Malawi
8)Oleg Yurievich Latyshev IMA academy president

2. Corresponding author: luisetto m maurolu65@gmail.com italy 29121 zip
code
Chapther 1 Abstract
Aim of this work is to verify difference in spread attitudes of covid-19 and
other coronavirus versus Smalpox and try to seek rational explain of the
specific pattern of diffusion.
The rapid increase of covid- 19 cases in FRANCE in second wave in fisrt
day of october 2020 seem to follow not only a diffusion related direct
contact and by droplet but also by airborne trasmission.
A real fact is the diffenece in size of virus smalpox vs coronaviruses.
Virus size is an relevant factor involved in kind of spread.
Keywords : COVID-19 , CORONAVIRUS , SMALPOX , RESPIRATORY
VIRUS, SPREAD, DIFFUSION , AIRBORNE ,WIND EFFECT, TIME OF
SPREAD, VENTILATION EFFECT
Chapther 2 Introduction

3. Related covid-19 pandemia it is interesticg to notice that many document
related past SPANISH FLU was extremely similar to nawadays allert
produced by public intrnational health organization to prevent spread of
this dangerosu disease ( see fig. 1)
Fig.n 1 Chicago theaters displayed posters like this one to slow the
spread of the Spanish flu during the 1918 pandemic.
At the same time it is interesting to observe the difference in size of
some respiratory virus : from the more great size of smallpox to the
small SARS virus.
This variability in size can be responsible of the different kind of diffusion
of this virus?
Smallpox more diffused by direct contact and by droplets then other
coronavirus and this instead seem involved also in airborne
transmission.

4. The kinetics of the diffusion of this virus seem to tell us that in the cases
of covid.19 second wave in France where numerous cases increased
but in very rapid ay ( weeks) in October 2020 is a patter different to the
spread of smallpox diffusion in north America in 1781 in HUSTON BAY
.
FIG. N. 2 virus size and dimension ( variola – smallpox)
Chapther 3 Material and methods
Whit an observational methods some relavant maps and images related
some respiratory virus diffusion in the world are analysed .
Also some literature involved and useful to this topic is presented in order
to produce a global conclusion
Fact-related.

5. All literature comes from Pub med or other open science journal .
It is used in this work a VISUAL method to find the final conclusion and
some relevant figure are reported.
Various respiratory virus are analyzed and also covering since smallpox
epidemy in north america after columbus travel.
Chapther 4 Results
In this section are reported relevant figure involved in respiratory virus
diffusion:
Related kind of spread, timing, velocity of the process.
we do know that the airborne -transmission has been shown to be a predominant route- way of
transmission for a number of communicable kind of diseases, including the rhinovirus and
influenza.

6. Fig. n 3

7. Fig. n. 4 10 march 2020 The locations of people who have tested positive
covid-19 in the U.S.
Source The new York times

8. Fig. n 5 USA population 2016

9. Fig.n 6 covid cases September 2020 from jama network

10. Fig. n 7 form Business insider
Fig n 8 H1N1 Swine Flu Spread June 2014 form
Rachael Rettner, LiveScience

11. FIG. n 9
Amos Ssematimba et al:
“We calculate the distance-dependent probability of infection for farms down-
wind of an infected farm by combining our model predictions of the hourly
depositions with the virus amount and infection probability models, the
inhalation-model and the within-flock epidemic model as described in
the Materials and Methods section. We use the Dutch 2003 epidemic data to test
whether wind-borne HPAI spread was possible and if so, determine its possible
contribution during the epidemic by comparing our model -predictions with the
observed pattern in the epidemic. As can be seen from equations reported , for
small infection- probability per inhalation the model-predicted probabilities are
to a very good approximation proportional to the deposition pattern . As a result,
in the parameter range of interest here, the distance-dependence of the model-
predicted probabilities is practically indistinguishable from that of the
deposition- pattern.
The comparison in figure reported more importantly shows a qualitative
difference in the tail. Compared to the observed pattern, there is a faster drop in

12. the predicted infection probability beyond 0.45 km. At all distances from the
source, the predicted probabilities are smaller than the observed- risk. Also,
beyond 1 km distance the predicted risk of solo wind-borne infection is decaying
significantly- faster with distance than the observed -risk. The observed rapid
decrease of the predicted -risk with distance is only very weakly sensitive to the
precise value of pathogen -decay rate, settling velocity and the within-flock basic
reproduction ratio as shown in figure reported. Based on these results, we
conclude that the wind-borne route alone could not explain the pattern of the
2003 -epidemic.”
Fig. n 10 Spanish flu 1918 spread and death

13. Fig. n 11 SPANISH FLU 1918 SPREAD
Fig. n 12 HONG KONG flu 1968 diffusion

14. Fig. n 13 smalpox spread USA case of smallpox during the 1775-82
epidemic.
The strange truth about smallpox and Native Americans
Posted on June 15, 2019 Memories of the people
“Did Europeans deliberately give smallpox-infected blankets to Native-
Americans? Absolutely. There is 1 proven case and many other suspicious ones.
But the largest smallpox outbreak, the one that killed possibly hundreds of
thousands of Natives, started during the Revolutionary -War. While the war
naturally brought people – and the virus – together and then re-distributed them,
the virus was also spread when the British- army, most of whom had already
been exposed to the disease, deliberately tried to infect American- colonists with
smallpox.”

15. Figure n 14 smallpox 1837
https://alchetron.com/1837-Great-Plains-smallpox-epidemic:
“The 1837 Great Plains smallpox- epidemic spanned from 1836
through 1840, but reached its height after the spring of 1837 when an
American Fur- Company steamboat, the S.S. St. Peter, carried infected
people and supplies into the Missouri- Valley area . More than 15,000
Native -Americans died along the Missouri River alone, with some tribes
becoming nearly extinct. Having witnessed the effects of the epidemic on
the Mandan -tribe, fur trader F. Chardon wrote, "the small-pox had never
been known in the civilized- world, as it had been among the poor
Mandans and other Indians tribu’. Only twenty-seven Mandans were left
to tell the tale.

16. Smallpox has afflicted the Native- Americans since it was carried to the
western- hemisphere by the Spanish conquerors, with credible accounts
of epidemics dating back to at least 1515. The Mandan -tribe, also
named the People of the Pheasants, had previously experienced a major
smallpox -epidemic in 1780-81 which severely reduced their numbers
down to less than a few- thousand. Many other tribes along the Missouri -
river suffered smallpox- epidemics during 1801-02 and 1831”
From CDC resource :
Origin of Smallpox
“The origin of smallpox is unknown. Smallpox is thought to date back to
the Egyptian -Empire around the 3rd century Before Common- Era ,
based on a smallpox-like rash found on three mummies. The earliest
written- description of a disease that clearly resembles smallpox
appeared in China in the 4th century Common- Era. Early written
descriptions also appeared in India in the 7th -century and in Asia Minor
in the 10th- century
17th -Century – European colonization imports smallpox into
North of America.
Old World, the most common form of smallpox killed perhaps 30 %
of its victims while blinding and disfiguring many others. But the
effects were even worse in the Americas, which had no exposure to
the virus prior to the arrival of the Spanish and Portuguese-
conquistadors. Tearing through the Incas before F. Pizarro even got
there, it made the empire unstable and ripe for conquest. It also
devastated the Aztecs populations , killing, among others, the
second-to-last of their rulers. In fact, historians believe that
smallpox and other European diseases reduced the indigenous
population of North and South -America by up to 90 %, a blow far
greater than any defeat in battle. “
“ the Smallpox -patients became contagious once the first
sores appeared in their mouth and throat (early rash-

17. stage). They spread the virus when they coughed or sneezed
and droplets from their nose or mouth- spread to other people.
They remained contagious until their last smallpox- scab fell off.
These scabs and the fluid found in the patient’s -sores also
contained the variola -virus. The virus can spread through
these materials or through the objects contaminated by them,
such as bedding or clothing. People who cared for smallpox -
patients and washed their bedding or clothing had to wear
gloves and take care to not get infected.
Rarely, smallpox has spread through the air in enclosed – kinds
of settings, such as a building (airborne- route).
Smallpox can be spread by humans only. Scientists have no
evidence that smallpox can be spread by the insects or
animals.”
Smallpox: Emergence, Global Spread, and Eradication
Frank Fenner 1993

19. Ann M.Carlos et al :
“The route of infection is the respiratory tract
This requires direct -contact with an infected person, and transmission, with rare
exceptions, through inhaled liquid -droplets. Unlike measles, patients with
smallpox do not generally have respiratory symptoms such as coughing or
sneezing which generate large clouds of infection in the air. As a result, “direct
and fairly prolonged face-to-face contact is required to spread the disease from
one person to another,” usually contact within about 6 to seven 7 for a period of
a few hours (CDC, 2010, “Smallpox Disease Overview”). Although droplets or
scabs that fall on bedding or clothing remain infectious in principle, laboratory -
tests using vaccinia virus indicate that infection is unlikely because of how the
material is handled by the respiratory- tract. Also, in experiments on the
persistence of infectivity, it has been found that the virus is rapidly inactivated,
even on heavily contaminated objects. There are instances of laundry- workers
contracting smallpox, but the documented cases of smallpox transmission via
fomites are very rare .”

20. Fign 15
Fig. n16 dengue pattern of spread form The new York times June 2019

21. Fig. n 17 from AWEA
In this figure it is interesting to observe the distribution of wind
manufacturing facilities in USA
( an indirect indicator of wind status)
Zhili Zuo et al :
“Normalized infectious virus -size distribution, total virus -size
distribution, SMPS particle number distribution, and SMPS particle
volume distribution for airborne MS2. Values are means ± one standard
n = 3). Similar plots for TGEV, SIV, and AIV are available online . To
better understand virus- transmission by aerosols, it is important to
determine the relationship between airborne virus infectivity/survivability

22. and particle size . Only a few studies are available on this issue in the
scientific- literature. To determine the distribution of infectious virus
among poly-disperse -particles, an Andersen cascade impactor was used
to sample aerosols of coxsackie virus A-21 and simian -rotavirus . The
concentration of infectious virus appeared to be related to particle volume
-distribution for particle size >0.5 μm. Using the same instrument, Appert
et al. (2012) confirmed the above findings for MS-2 bacteriophage, but
not for adenovirus. Tyrrell (1967) found that rhinovirus survived better in
coarse -particles (>4 μm) than in smaller particles (0–4 μm), while
adenovirus infectivity was best preserved in the size range of 0.56–1.9
μm compared with 1.9–10 μm indicating that particle -size may also
affect virus survivability. Although the use of size-segregated samplers,
such as impactors, provides size fractionation for virus infectivity, not
much is known about virus aerosol particles of human and animal-
viruses remains an issue . The objective of this study was to examine
infectivity and survivability of three airborne animal viruses as a function
of their carrier particle size in the submicron size- range using a newly
developed sampling method. In addition, the behavior of widely used
MS2 bacteriophage was studied for comparative purposes .Propagation
and Titration of MS2 Bacteriophage MS2 bacteriophage (ATCC 15597-
B1) is a small (27–34 nm), icosahedral, non-enveloped, single stranded,
positive sense RNA -virus, infecting only the male Escherichia coli (those
bearing an F pilus) . For the purposes of this study, we considered MS2
as a model virus because it has been widely used in many virus aerosol
studies . The virus was propagated in E. coli famp (ATCC 700891), as
described elsewhere . Briefly, 0.1 mL of MS2 and 1 mL of a log phase
culture of E. coli were added to top agar tubes held at 48◦C. After mixing,
the contents of the tubes were poured on trypticase soy agar (TSA)
plates. The top agar was allowed to solidify followed by inversion and
incubation of plates at 37◦C for 24 h. After plaques were confluent (within
24 h of incubation), 5 mL of tryptic soy broth (TSB) was added to each
plate. After 2 h at room -temperature, the solution was aspirated,
centrifuged at 2500 × g for 15 min, and sterile-filtered. The resulting
bacteriophage stock was aliquoted into 50 mL tubes, followed by storage
at −80◦C until use. The amount of MS2 -bacteriophage in virus stock and
various other samples was determined by using a double agar- layer
procedure as described elsewhere . The amount of virus was expressed

23. as plaque -forming units per unit volume of the sample (PFU/mL)”.
Fig. n 18 Schematic diagram of the experimental setup for the
characterization of virus aerosols.

24. Fig. n 19
“Four viruses MS2 -bacteriophage, transmissible gastroenteritis virus,
swine- influenza virus, and avian -influenza virus) were aerosolized, size
classified (100–450 nm) using a differential mobility- analyzer (DMA), and
collected onto gelatin filters. Uranine dye was also nebulized with the
virus, serving as a particle tracer. Virus -infectivity assay and quantitative
reverse transcription-polymerase chain reaction were then used to
quantify the amount of infectious virus and total virus present in the
samples, respectively. The virus -distribution was found to be better
represented by the particle -volume distribution rather than the particle
number distribution. The capacity for a particle to carry virus increased
with the particle- size and the relationship could be described by a power

25. law. Virus survivability was dependent on virus type and particle- size”
Nanomedicine Volume I: Basic Capabilities Robert A. Freitas Jr.
“Large Molecule -Binding, Sorting and Transport Is there any size limit for
target molecules to be transported?
Natural- receptors have already been found for large molecules including
low-density lipoproteins (LDLs) > 1,000,000 daltons426 and high-density
lipoproteins (HDLs).The methods described in earlier Sections can be
adapted for binding large- molecules (>1000 atoms; Fig. 3.15), including
molecules far wider than the binding device itself ( ~200-nm diameter
virus particles and larger). Making a binding site for a large molecule
should be physically easier (albeit computationally more challenging)
than making a binding -site for a small molecule because of the greatly
increased area of interaction.
In example, a binding energy of 400 zJ may be realized by creating a
dispersion-force binding -area covering only ~25% of the surface of a
10,000-atom target molecule or a mere ~0.02% of a 200-nm virus-
particle.
Assuming a roughly spherical large molecule and laminar fluid -flow at 1
atm forcing pressure (Section 9.2.7), a 10-nm diameter molecule moves
through a 20-nm long pump (~10-20 kg, ~106 atoms) in ~10(-6 )sec at
~0.02 m/sec, consuming ~0.02 pW during transfer.
A 200-nm virus-size target molecule moves through a 400-nm long pump
(~10-17 kg, ~109 atoms) in ~10 (-2) sec at ~60 microns/sec, consuming
~10-16 watts during transfer; at ~0.0002 atm, release- time is diffusion
limited.
The transfer force exerted on a 10-nm molecule is ~1 pN, ~600 pN on a
200-nm virion; a binding energy of 400 zJ at a 0.2-nm contact distance
gives a binding- force of ~2300 pN, sufficient to hold a particle of either
size firmly during transport and release” (4)
“As demonstrated previously, the particle size can significantly affect
survival of airborne viruses “ (3)

26. Zhili Zuo et al :
“Although laboratory generated virus- aerosols have been widely studied in terms of infectivity and
survivability, how they are related to particle- size, especially in the submicron- size range, is little
understood. Survivability of the three animal viruses at large particle -size (300–450 nm) was
significantly higher than at particle size close to the size of the virion (100–200 nm), which could
be due to the shielding -effect. The data suggest that particle size plays an important role in
infectivity and survivability of airborne viruses and may, therefore, have an impact on the airborne
transmission of viral illness and disease. The data in this study do not support the use of MS2 -
bacteriophage as a general surrogate for animal and human -viruses. (3)
Infectious/Total Virus Size Distribution
Figure reported represent the infectious virus and total virus -size distribution from 100 nm to

27. 450 nm normalized by the maximum- values. In general, both the infectious and total virus-
concentrations increased with particle size and the maximum -values at 400–450 nm were around
5000 PFU/cm3
, 35 TCID50/cm3
, 180 TCID50/cm3
, and 60 TCID50/ cm3
for MS2, TGEV, SIV, and
AIV, respectively, which were several orders of magnitude lower than the particle number
concentration at the same particle -size. The virus -size distributions were normalized to compare
them more easily with particle size- distributions. As seen in Figures reported , the infectious and
total virus distributions had a similar trend, both appearing to follow particle volume distribution
rather than particle number distribution. Infectious and total virus- concentrations collected by the
gelatin- filters are available on-line .
Survivability of Airborne Virus
“Similar to RRIV , survivability of TGEV and AIV was much lower at
200 nm than at larger -size . One could argue that the discretization
phenomenon is responsible for this finding, as the carrier particle- size
gets smaller and approaches the size of virion, it becomes more difficult
for the particle to carry virus. the particle- size-independent RRTV shown
in figure reported suggests the presence of virus in particles even at
100 nm. Therefore, the discretization phenomenon was probably not the
reason. The main reason for the particle -size associated survivability
could be the shielding- effect. More specifically, compared with virus
existing as a singlet or in association with fewer- organics (solutes in the
nebulizer -suspension), the virus at larger particles may be surrounded
by more organic- material, which may form a shield. Shielding -effect has
been demonstrated to better protect virus from environmental- stress
such as ultraviolet irradiation . It may also reduce sampling stress such
as desiccation and sampler dependent-mechanical forces, thus better
maintaining the infectivity of airborne -virus. as particle -size increased to
300 nm and above, virus survivability seemed to reach a plateau,
suggesting the shielding- effect was maintained once a specific particle -
size was reached. The same explanation applies to MS2. Because all
collected particle -sizes were more than four times the virion size (27–

28. 34 nm), the survivability reached the plateau -regime and therefore was
no longer depended on particle- size . This is supported by Lee (2009),
who showed that survivability of MS2 at 120–200 nm was higher than at
30 nm, despite the large experimental variation.” (3)
Fig. n. 20 Schematic representation of the shielding effect of the
hydration layer due to the presence of zwitterionic moieties. ( from
references)
Mahesh Jayaweera et al :

29. Behavior of droplets and aerosols against environmental factors
“The most important environmental- factors that could impact on the viability of airborne -microorganisms
are temperature, humidity, radiation (sunlight), and open-air (ventilation) . Most viruses, including SARS-
CoV-2, are less than 100 nm in size . Viruses in aerosols lose or gain the viability and infectivity because of
environmental -stresses caused by temperature, relative humidity, and sunlight before they reach a
susceptible host. Environmental -tolerance of the virus-laden aerosols depends on the specific- phenotype
available, the composition of the bioaerosols containing virus and their payload, and physical -
characteristics in the surrounding environment . As the environmental- factors play a major role in
transmitting payloads of SARS-CoV-2 virus in different geographical -locations of outdoor and indoor -
environments, it is worthy of exploring the effects of environmental factors on the transmission of SARS-
CoV-2 virus. there have been associations between air -pollution represented by air pollutants such as
PM2.5, PM10, NO2, and O3 and COVID-19 infection ” (6)
Wan Yang et al :
“The concentrations and size -distributions of airborne influenza -viruses were measured in a
health centre, a day-care facility and aeroplanes by qRT–PCR. During the 2009–2010 flu season,
50 per cent of the samples collected (8/16) contained IAVs with concentrations ranging from 5800
to 37 000 genome -copies m−3. On average, 64 per cent of virus-laden particles were found to be
associated with particles smaller than 2.5 µm, which can remain airborne for hours. Modelling of
virus concentrations -indoors suggests a source strength of 1.6 ± 1.2 × 105 genome copies m3 h
−1 and a deposition flux onto surfaces of 13 ± 7 genome copies m−2 h−1. Doses of 30 ± 18, 236
± 140 and 708 ± 419 TCID50 were estimated for 1, 8 and 24 h exposures, respectively. As a
whole, these results provide quantitative support for the possibility of airborne -transmission of
influenza “(7)
Luis A. Anchordoqui et al :
“ MODELING THE EFFECT OF CONVECTION -CURRENTS IN THE TRANSMISSION OF
SARS-COV-2 In the presence of air resistance, compact heavy objects fall to the ground quickly,
while light objects exhibit Brownian -motion and follow the pattern of turbulent- convection of the
air. For aerosol -particles containing the virus, the boundary between these two behaviors
depends on the size of the particle. We begin with a simple question: how long does a virus float
in the air under the influence of gravity? To answer this query we model the virus as a sphere of
radius r ∼ 90 nm and mass m ∼ 2.5×10−19 kg, and we assume that this spherical- particle is
suspended in a viscous fluid (the air) feeling the Earth’s gravitational field. Herein, gravity tends to
make the particles settle, while diffusion and convection act to homogenize them, driving them
into regions of smaller concentration. On the one hand, the convection mechanism provides
particle macro-mixing within the fluid through the tendency of hotter and consequently less dense
material to rise, and colder, denser material to sink under the influence of gravity. On the other
hand, the diffusion -mechanism acts on the scale of an individual particle (micro-mixing) slowly

30. and randomly- moving through the media. Under the action of gravity, the virus acquires a
downward terminal speed that follows from Stokes law.
is the virus -mobility in the fluid, and where η = 1.8 × 10−5 kg/(ms) is the dynamic viscosity of air .
Substituting (2) into (1) we find that the downward terminal speed of the virus in dry air is indeed
negligible, vdown ∼ 8 × 10−8 m/s. It is therefore clear that gravity plays no role in the motion of an
isolated -virus through the air. Rather it follows a convection pattern in a manner similar to how
smelly- substances move through the air. The survival probability of the virus in the dry- air is then
given by the likelihood of survival outside its natural -environment. The half-life of SARS-CoV-2 in
aerosols has been found to be about 1.1 hours . For large droplets whose diameters & 1000 µm,
the effect of air -resistance is negligible and so the falling time can be directly estimated using
Newton’s equations for gravitational settling. For smaller droplets whose diameters < 100 µm, the
falling times must instead be determined using the downward terminal- speed given in (1) to
account for the air resistance upon the falling droplets. It is now an instructive and straightforward
exercise to show that the time for falling 2 m in saturated air is 0.6 s for droplets with r > 500 µm,
6.0 s for those of r ∼ 50 µm, 600 s (about 10 minutes) for those of r ∼ 5 µm, and 60,000 s (about
16.6 hours) for those of r ∼ 0.5 µm. The droplet evaporation -time scale, as computed by Wells
using droplet “(8)
Rajiv Dhand et al :
“In respiratory- exhalation flows, the large droplets between 60 and 100 mm in size are expected
to completely evaporate before traveling 2 m (30). These large droplets are carried farther away
when they are expelled at high -velocity, such as with coughs and sneezes. The time it takes
particles to fall to the floor depends on their size; particles 100 mm in diameter take about 10
seconds, whereas 10-mm–diameter particles are estimated to take 17 minutes to fall to the floor,
and 1- to 3-mm–diameter particles could remain suspended almost indefinitely especially if they
are periodically elevated by air -current (VERNON KNIGHT 1980 “) .
Aerosols, Droplets, and Airborne Spread: Everything you could possibly want to know
Justin Morgenstern:
As is discussed below, this form of aerosolization is thought to have spread
SARS in the Amoy -Garden apartment complex in Hong Kong. (Morawska
2006)
However, whether these aerosols are capable of transmitting disease still
depends heavily on the number produced, the concentration of the infectious -
agent, the virulence of the microbe, environmental -factors (the virus needs to be
able to survive, whether in the air or on a surface, until it enters a host), and the
health and immunity of the host. (Morawska 2006) As I said, exact size -cutoffs

31. are controversial, but Chen (2010) suggests that the distribution of all droplets
between 0.1 and 200 µm will primarily be influenced by ventilation- patterns
and the initial velocity of the droplet, rather than gravity. In other words, these
droplets do not just drop to the ground within 1-2 meters of the patient, as many
infection control practices assume., the distribution of droplets is also influenced
by a very large number of factors, including relative humidity, temperature,
ventilation pattern and rate, initial- velocity, shape of the human body, and
droplet nuclei -size and composition. (Xie 2007; Chen2010) Most of these
factors are dynamic (droplet- size changes as it evaporates and temperature
changes as you move away from a febrile- patient), making simplified
calculations difficult. At smaller -sizes, Brownian motion, electrical forces,
thermal gradients, and turbulent diffusion have much bigger impacts. (Morawska
2006) Overall, it is complicated, there are lots of formulas, and reading these
papers generally left me with a headache.Any infection that behaves like
influenza could easily be spread through- aerosols.
Aerosols are tiny and their concentration -drops off exponentially as you get
farther from the source (especially with good- ventilation). Of course we don’t
frequently see transmission over large- distances or large -scale outbreaks. The
chances of encountering viable virus across the room are just too lw.
that line of reasoning completely discounts close range aerosol- spread. Aerosols
will be most concentrated within a few meters of the patient. At that distance,
aerosol spread is almost indistinguishable from droplet -spread. In fact, it is
generally completely ignored, because many people just assume that short range
spread is due to droplets. short range -aerosol spread would have significant
implications for our PPE -choice

32. Fig. n : 21 from Characteristic size ranges of atmospheric particles and
bioaerosols (A) protein (B) virus, (C) bacteria, (D) fungal spore and (E) pollen
grain (Fröhlich-Nowoisky et al. 2016)
Fig. n. 22 size some virus and PM

33. Fig. n. 23
Transmission and control of viruses via infectious droplets and aerosols in indoor environments
Theodore A. Myatt et al :
“We detected airborne -picornavirus in 32% of air sampling -filters in office buildings using
molecular methods. We show a significant positive relationship between the frequency of virus
detection in air- filters and degree of building ventilation with outdoor- air as measured by average
CO2 concentrations greater than 100 ppm above the background. Thus, these data suggest that
lower ventilation -rates and resulting increased CO2 concentrations are associated with
increased- risk of exposure to potentially infectious droplet- nuclei. (10)”
Martin Meyer Weiss et al :
“If one assumes that influenza is transmitted by respiratory- droplets (> 10 μm in size, which
immediately fall to the ground) rather than by aerosols (< 10 μm in size, which remain suspended
in air for long -periods of time)” (11)
Larisa Anghel et al :
“Pulmonary- activities such as coughing , breathing , sneezing or talking, are sources of bio-
aerosols that can have respiratory tract infections pathogens . Large droplets (>10 microns),
formed especially from coughing and sneezing, fall on surfaces and objects not further than 1–2
m from the infected -patient. People can catch the infection directly by standing within 1–2 meters
of an infected person and breathing in these droplets. When people are standing within 1–2
meters of an infected -patient or when they touch their mouth, nose or eyes after they touched the

34. contaminated -surfaces or objects, they can catch the infection . Droplets that evaporate (10
microns droplets evaporate in 0.2 s) and desiccate, form small particles (droplet nuclei or
residue). Aerosols are small-particles (< 5 microns )
with a slow velocity and may remain suspended in the air for hours and can be transported long
distances” (12)
Natalie Pica et al :
“Viral- infections of the respiratory tract are common acute illnesses among humans, and virus-
transmission, by either direct or indirect routes, occurs in disparate regions around the globe. A
more detailed understanding of how these viruses transmit can have broad public health
implications. Indeed, a variety of meteorological factors have at times been associated with rates
of virus infection as well as transmission among- individuals. As presented in this review,
precipitation, humidity, temperature, and airflow can be determinants of virus infection and
transmission; despite robust investigation of the effects of these environmenta-l factors,
inconsistencies and uncertainties in the data remain. It is possible that meteorological -
determinants play greater roles in some geographic- regions than others, or simply that
differences in experimental design affect outcomes and data interpretation. Non-environmental
effects, including but not limited to seasonal- changes in behavior, family and social structures,
and pre-existing immunity, could also be playing a role in respiratory virus t-ransmissibility and
rates of infection. Discrepancies in collected data suggest that more vigilant surveillance over
large geographic regions and further controlled experiments in animal -models and perhaps in
humans will probably be necessary to determine with increased certainty the role that
environmental factors play on the transmission of viral -pathogens.” (13)
Aaron Fernstrom et al :
“airborne- transmission is defined as the transmission of infection by expelled particles that are
comparatively smaller in size and thus can remain suspended in air for long- periods of time.
Airborne- particles are particularly worrisome simply because they can remain suspended in the
air for extended periods of time. Seminal studies from the 1930s and 1940s demonstrated that
airborne particles can remain airborne for as long as one week after initial- aerosolization, and
suggested further that these particles likely remained airborne for much longer. They thus
potentially expose a much higher number of susceptible- individuals at a much greater distance
from the source of infection . Depending on environmental- factors ( meteorological conditions
outdoors and fluid dynamic effects and pressure differentials indoors), airborne- particles are
easily measured 20 m from their source . These factors would be of no concern but for the fact
that airborne bacterial, viral, and fungal particles are often infectious . Exposure to airborne
pathogens is a common denominator of all human life . With the improvement of research-
methods for studying airborne pathogens has come evidence indicating that microorganisms
(e.g., viruses, bacteria, and fungal spores) from an infectious- source may disperse over very
great distances by air currents and ultimately be inhaled, ingested, or come into contact with
individuals who have had no contact with the infectious -source . Airborne pathogens present a
unique challenge in infectious -disease and infection -control, for a small percentage of infectious
individuals appear to be responsible for disseminating the majority of infectious- particles . (14)

35. Chapther 5 Discussion
Is possible to verify the difference in spread of virus smallpox – variola (
high dimension) versus other small virus in USA maps .
Observing pattern of diffusion in 1870 in BAY of HUSTON is possible to
verify the time ( month) necessary to spread and this reflect correctly a
diffusion by direct contact or droplets.
Instead COVID-19 diffusion especially in second wave in France in
October 2020 seem to follow other model : a logarithmic explosion of
cases in a few week:only direct contact od droplets or other factors acts (
airborne diffusion ?)
Observing the spread of covid-19 , SARS, seasonal flu and suine flu it is
clear that there is a not omogenea
Pattern of diffusion in all USA STATES whit a GRADIENT ( more involved
east region then centre of USA)
The spread of smallpox in North America followed a gradient also from
east to west but in more slowly way.
Even if nowadays modern travel system ( airplane , train, cars and other )
the spread of coronavisus covid-19 in march 2020 in NORTH America
followed a determinate gradient versus .
“Virus survivability was dependent on virus type and particle size”
According WHO : Airborne transmission is defined as the spread of an infectious agent
caused by the dissemination of droplet- nuclei (aerosols) that remain infectious when suspended
in air over long- distances and time.

36. Particulate matter (PM) in the air, whether in solid or liquid -
form, can affect our health. Particularly those particles of below
2.5 micrometers (microns; μm) represent a hazard, as they are
able to enter our blood-stream. Nano-particles can be as small
as 0.1 right down to 0.001 μm.
Sizes of Influenza A virus: about 0.08 - 0.12 μm
The coronavirus species COVID-2019, MERS-CoV and SARS-
CoV range in size from about 0.06 to 0.2 μm
Some effect influence particles suspended in the air like Brownian –moto.
This Brownian motion ( A. EINSTEIN 1905) is a random motion of particles suspended in a
medium (a liquid or gas).
A random -fluctuations in a particle's position inside a fluid sub-domain, followed by a relocation to
another sub-domain. Each re-location is followed by more- fluctuations within the new closed -
volume.
Molecules of a fluid , under termic- shaking , produce casual moto of a particle inside this.
This fluctuation influence the particle in higher -way when this is of lower -size the higher
ones.
In example For larger- particles, the HEPA -filter acts like a net
as we would expect. Particles greater than about 0.3 μm in size
simply cannot get through: either they do not fit through the
holes or they hit the filter- fibers due to inertia. For the smaller-
particles, it would seem logical that they can simply go through
the holes. ( this is not the case) . The tiny- mass of particles
less than about 0.3 μm means they do not fly straight; instead,
they are bounced off other molecules as they collide with them
and thus move in completely random -patterns. As a result,
they hit the filter -fibers and then remain stuck in them. This is
the principle of the Brownian- movement phenomena.

37. Chapther 6 Conclusion
Related the figure and reference reported in this work it is possible to
conclude that is seem that related also to the size of respiratory virus the
pattern of diffusion ( time and versus ) is different.
According literature AIRBORNE virus spread and transmission is function
of various factors : carrier size , virus size , distance , time , subject
characteristic, phisiopathologic patient condition , air pollution level,
temperature, humidity ,air flux , Brownian moto, air current and other .
Spreading and diffusing of the virus are definitely associated or
correspond with virus size and airborne mechanism.
Of this observation public authorities must take in consideration.
Source of founding : self
Conflict of interests: none
Ethical consideration: this work is produced under all ethical rules for this
kind of research
Clarifications: this work is produced with put any diagnostic or
therapeutic intent , only to submit to the researcher a new theory

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