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  <front>
    <journal-meta>
      <journal-title-group>
        <journal-title>San
Diego, California, USA, August</journal-title>
      </journal-title-group>
    </journal-meta>
    <article-meta>
      <title-group>
        <article-title>A New Delay Differential Equation Model for COVID-19</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <string-name>B Shayak†</string-name>
          <email>sb2344@cornell.edu</email>
          <xref ref-type="aff" rid="aff1">1</xref>
        </contrib>
        <contrib contrib-type="author">
          <string-name>Mohit M Sharma</string-name>
          <email>mos4004@med.cornell.edu</email>
          <xref ref-type="aff" rid="aff2">2</xref>
        </contrib>
        <contrib contrib-type="author">
          <string-name>Manas Gaur</string-name>
          <email>mgaur@email.sc.edu</email>
          <xref ref-type="aff" rid="aff0">0</xref>
        </contrib>
        <contrib contrib-type="author">
          <string-name>Retarded logistic equation, Asymptomatic carriers, Latent</string-name>
          <xref ref-type="aff" rid="aff3">3</xref>
        </contrib>
        <aff id="aff0">
          <label>0</label>
          <institution>AI Institute, University of South Carolina</institution>
          ,
          <country country="US">USA</country>
        </aff>
        <aff id="aff1">
          <label>1</label>
          <institution>Mechanical and Aerospace Engg, Cornell University</institution>
          ,
          <addr-line>Ithaca, New York State</addr-line>
          ,
          <country country="US">USA</country>
        </aff>
        <aff id="aff2">
          <label>2</label>
          <institution>Population and Health Sciences, Weill Cornell Medicine</institution>
          ,
          <addr-line>New York City</addr-line>
          ,
          <country country="US">USA</country>
        </aff>
        <aff id="aff3">
          <label>3</label>
          <institution>transmission</institution>
          ,
          <addr-line>Contact tracing, Reproduction number calculation, Partial herd immunity</addr-line>
        </aff>
      </contrib-group>
      <pub-date>
        <year>2020</year>
      </pub-date>
      <volume>24</volume>
      <issue>2020</issue>
      <abstract>
        <p>In this work we give a delay diferential equation , the retarded logistic equation, as a mathematical model for the global transmission of COVID-19. Th is model accounts for asymptomatic carriers, pre-symptomatic or latent transmission as well as contact tracing and quarantine of suspected cases. We find that the equation admits varied classes of solutions including self-burnout, progression to herd immunity and multiple states in between. We use the term “partial herd immunity” to refer to these states, where the disease ends at an infection fraction which is not negligible but is significantly lower than the conventional herd immunity threshold. We believe that the spread of COVID-19 in every localized area can be explained by one of our solution classes.</p>
      </abstract>
    </article-meta>
  </front>
  <body>
    <sec id="sec-1">
      <title>-</title>
      <p>Retarded logistic equation</p>
    </sec>
    <sec id="sec-2">
      <title>CCS CONCEPTS</title>
      <p>• Applied computing – mathematics and statistics</p>
    </sec>
    <sec id="sec-3">
      <title>1 Introduction</title>
      <p>Three kinds of models to study COVID-19 are currently in
vogue – lumped parameter or compartmental models (ordinary
differential equation), agent-based models and stochastic
differential equation models. The first option affords maximum
conceptual clarity at the expense of some simplifying assumptions
†Presenting author, Corresponding author. ORCID : 0000-0003-2502-2268
(homogeneous mixing etc). The second option affords maximum
potential versatility at the cost of huge computational complexity
and variability in the network structure. The third option
combines features of the previous two – whether the features
being synergized are the positive or the negative ones depends to
a large extent on the modeler.</p>
      <p>
        In this work we use delay differential equations (DDE) to
propose a simple, single-variable, lumped parameter model for the
spread of Coronavirus. Jahedi and Yorke [
        <xref ref-type="bibr" rid="ref1">1</xref>
        ] make a strong case
for simpler models relative to complex and elaborate ones. In the
Literature, DDE has been used for modeling COVID-19, for
example in Refs. [2]–[4]. These authors however ignore features
such as contact tracing, asymptomatic carriers and latent
transmission; our results too have a richer structure.
      </p>
      <sec id="sec-3-1">
        <title>2 Derivation of the model</title>
        <p>We measure time t in days and use as our basic variable y(t)
which is the cumulative number of corona cases, including active
cases, recovered cases and deaths, in the region of interest. The
following “word-equation” summarizes the approach :
 Rate of emergence   Interaction rate of 
  =   
 of new cases   each existing case 
 Probability of   Number of 
    
 transmission   existing cases 
persons/day. For a compartmental model, one must average over
the professor, the grocer and all the other un-quarantined cases to
generate an effective per-case interaction rate q0.</p>
        <p>Every interaction of course does not result in a transmission –
there is a probability strictly less than unity that the virus jumps
from the infected person to the person whom s/he is interacting
with. This probability has two components. The first component
is that the healthy person must be susceptible to begin with. While
we ignore intrinsic insusceptibles, there will be people who have
recovered from the disease and are therefore not susceptible
again. In this Article, we assume that one bout of infection brings
permanent immunity. The assumption is valid so long as the
immunity period exceeds the total epidemic duration. Till date,
there is little credible evidence for re-infection [5]–[7]; contrarily,
a very recent and thorough study [8] based on monitoring of huge
patient cohort has found significant evidence of long-lasting and
effective antibodies. If N be the initial number of susceptible
people (recall that y is the case count), then the probability that a
random person is a recovered case is approximately y/N and the
probability that s/he is susceptible is (approximately) 1−y/N. This
expression is approximate because the true number of recovered
cases at any time is less than y; the error however is small since
the recovery period is much shorter than the overall course of the
epidemic. Note that 1−y/N is a logistic term, and a herd immunity
effect.</p>
        <p>Given susceptibility, the next probability is that the virus
actually does jump from the un-quarantined case to the
susceptible person. This probability depends on the level of
precaution such as face covering or mask, handwashing and
disinfection being adopted by the case as well as the susceptible
person. For a compartmental model, the probability must be
averaged over all the un-quarantined cases. If this average
probability is P0, then q0(1−y/N)P0 gives the per-case spreading
rate. Since q0 and P0 are both dependent on public health
measures, and are both difficult to measure independently, we can
club those two together into a single parameter which we call m0.</p>
        <p>So far we have accounted for the rate at which each cases
spreads the disease; now we have to count the number of cases
out of quarantine. Let us start with an asymptomatic carrier, who
remains in open society throughout. S/he typically transmits the
disease for 7 days, which is called the infection period. Then, new
healthy people can be only be infected by those asymptomatic
cases who have fallen sick within the last 7 days, and not those
who have fallen sick earlier. The number of such people is the
number of asymptomatic sick people today minus the number of
those 7 days earlier. Mathematically, let μ1 (between 0 and 1)
denote the fraction of asymptomatic carriers and τ1 the
asymptomatic infection period. Then, the number of
asymptomatic transmitters today is μ1(y(t)−y(t−τ1)). Here we can
see the emergence of the delay term.</p>
        <p>The remaining fraction 1−μ1 of cases are symptomatic. Let τ2
be the latency period during which these cases remain
transmissible prior to displaying symptoms. It is assumed that
they isolate themselves thereafter. Assumption is also made that
the incubation period is equal to the latency period. Finally, the</p>
      </sec>
      <sec id="sec-3-2">
        <title>3 Solutions of the model</title>
        <p>Due to complexity of the equation (2), analytical solution using
perturbation theory etc has not been attempted in this case.
Instead we have used numerical integration to obtain the
solutions of (2). Before giving the solutions however, we present
the calculation of the reproduction number R. To find R at any
state of evolution of the disease, we first treat y in the logistic term
to be constant, and then carry out the steps described in Ref. [9].
This yields the expression</p>
        <p>R = m (1 −
0
y ) ( 1 + μ3 − 2 μ1 μ3 τ + μ μ τ )</p>
        <p>2 1 3 1</p>
        <p>N 2</p>
        <p>The ease of calculating R with respect to the ordinary
differential equation based models [10] is noteworthy.</p>
        <p>Solution classes of logistic DDE (2) are now demonstrated. The
numerical integration routine used is second order Runge Kutta
with a time step of 1/1000 day. As the testbed for the simulations,
we consider a Notional City having N=300000, μ1=0.8, (maximum
. (3)
contact tracing drive conducted by public health department is
taken into account. Assumption is made that this drive is
instantaneous and proceeds in forward direction starting from
freshly arriving symptomatic cases. The contact trace captures
patients who were exposed to the new case τ2 days ago, as well as
patients who were exposed immediately before the new case
manifested symptoms. The average duration for which these
secondary patients have remained at large is τ2/2, be they
symptomatic or asymptomatic. The assumption of instantaneous
contact tracing, which decreases the average time that
contacttraced cases spend out of quarantine, opposes the error arising
from the assumption of zero non-transmissible incubation period,
which increases the average time for which the contact-traced
cases transmit before quarantine. These two effects are assumed
here to cancel. Let μ3 (between 0 and 1) denote the fraction of all
cases who escape from contact tracing drives – the
complementary fraction 1−μ3 get caught. Thus, we have three
classes of un-quarantined cases : (a) 1−μ3 are contact-traced cases
who remain in society for a time τ2/2, (b) μ3 (1−μ1) are untraced
symptomatic cases who go into isolation only after time τ2, and (c)
μ3μ1 are undetected asymptomatic cases who transmit for the
entire infection period τ1. Arguments similar to those of the
previous paragraph yield the total number of un-quarantined
cases as
n = (1 − μ3 ) ( y − y (t − τ 2 / 2) ) +
( (1 − μ1 ) μ3 ) ( y − y (t − τ2 ) ) + μ1 μ3 ( y − y (t − τ1 ) )
The preceding arguments now yield the mathematical form of
(0) as
dy
dt
= m</p>
        <p>
0 
1 −
y   y (t ) − (1 − μ3 ) y (t − τ2 / 2) −

N  (1 − μ1 ) μ3 y (t − τ2 ) − μ1 μ3 y (t − τ1 ) 

(2)
which is the retarded logistic equation.</p>
        <p>. (1)
value as per our knowledge [11]–[13]), τ1=7 days and τ2=3 days
[14]. The initial condition needs to be a function having the length
of the maximum delay involved in the problem, which is seven
days; we take this function to be zero cases to start with and
constant increase of 100 cases/ day for a week.</p>
        <p>Notional City A has m0=0.23 and μ3=1/2, which describes a
hard lockdown [15] accompanied by good contact tracing. R0 (i.e.
(3) evaluated at y=0) is 0.886. The epidemic ends with a negligible
fraction of infected people, as shown below. This and the next five
plots are three-way – each plot shows y as blue line, its derivative
y as green line and the weekly increments in cases, or
epidemiological curve, as a grey bar chart. These last have been
reduced by a factor of 7 to ensure clarity of presentation. We
report the rates on the left hand side y-axis and the cumulative
cases on the right hand side y-axis.</p>
        <p>This is exactly what has happened in New Zealand – that il
fortunatissimo per verita has indeed quashed the epidemic
completely with the final case count being a negligible fraction of
its total (tiny and sparsely distributed) population.</p>
        <p>The parameter values for Notional City B are the same as those
for A except that μ3=0.75; a greater fraction of cases escape the
contact tracing drive. R0 is 1.16, and R becomes 1 at y=40500 cases.</p>
        <p>The outbreak enters exponential regime right after being
released. As y increases, R gradually reduces so the growth slows
down until it peaks when the case count is about 39,000 [compare
with the value of 40,500 when R=1 as per (3)]. Thereafter, the
disease progresses to extinction in time. The overall progression
is very long but one hopes that the relatively small size of the peak
can prevent overstressing of medical care facilities and thus avoid
unnecessary deaths. Delhi and Mumbai in India and Los Angeles
in USA are in all probability cities of this type since the disease
there spiraled out of control despite hard lockdowns being
imposed at an early stage.</p>
        <p>City B also enables us to explain partial herd immunity. Even
though the initial conditions were unfavourable for containment
of the epidemic, herd immunity started activating as the disease
proliferated. A stable zone (R&lt;1) was entered when only 13.5
percent of the total susceptible population was infected, and a
similar percentage again got infected before the epidemic ended.
Thus, herd immunity worked in synergy with
nonpharmaceutical interventions to stop the epidemic at only 26
percent infection level, which is significantly less than the
conventional 70-90 percent threshold [16]. This is what we call
partial herd immunity. Our findings are in agreement with and act
as an explanation for what has been obtained by Britton et. al. [17]
and Peterson et. al. [18].</p>
        <p>We now consider Notional City C which differs from City B in
that m0=0.5; lockdown is replaced by a much more permissive
state. R0 is above 2.5; 1,80,000 infections are required to bring it
below unity.</p>
        <p>Figure 3 : City C goes to herd immunity – total not
partial. The symbol ‘k’ denotes thousand and ‘L’ hundred
thousand.</p>
        <p>Need one mention that this is a public health disaster. Notional
City D combines features of B and C. This city begins with m0=0.5
like City C but reduces to m0=0.23 like City B when the case count
reaches 40,000 (the R=1 threshold for B’s parameters).</p>
        <p>Figure 4 : As the input, so the output – D’s response
combines features of B and C. The symbol ‘k’ denotes
thousand and ‘L’ hundred thousand.</p>
        <p>We can see a case count as well as a total duration intermediate
to B and C; the epidemic is over in 70 days but the peak rate of
12,920 cases/day is still very high and likely to load hospital
facilities beyond their carrying capacity.</p>
        <p>The Cities E and F demonstrate the issues faced in reopening.
In both these cities, the parameters and case trajectory are
identical to those of City A for the first 80 days. Then, E and F
reopen on the 80th day by increasing m0 from 0.23 to 0.5, and
simultaneously decreasing μ3 i.e. deploying a more effective
contact tracing program which had been built up during the
lockdown. The post-reopening μ3’s for E and F are 0.1 and 0.2
respectively.</p>
        <p>The difference between Cities E and F is dramatic.
Mathematically, R remained less than unity throughout in E; its
value after reopening was 0.985. We can see that the case rate
decreases monotonically all the time. In F, the post-reopening R
became 1.22 and sent the trajectory haywire. In practice however,
the incipient increase in case rate after the 80th day acts as an
advance warning of what has happened – the reopening steps
should be reversed if it is at all possible to do so while satisfying
economic and other external constraints.</p>
      </sec>
      <sec id="sec-3-3">
        <title>Conclusion</title>
        <p>In this Article we have presented a new mathematical model
for COVID-19 which is simple and elegant in structure but can
generate a variety of realistic solution classes. We hope that our
work may be of use to mathematicians and data scientists who are
trying to understand the spread of the disease in a quantitative
manner. The public health implications of these results are being
reserved for another study.</p>
      </sec>
    </sec>
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