The propagation of new viral infectious diseases can be described, to a first approximation, according to the SIR model developed by Kermack and McKendrick [1] [2] [3] [4] [5] [6] . In this deterministic compartmental model, three classes of individuals are considered:
Susceptibles, S, who can catch the disease; Infectives (infected and infectious), I, who can transmit the disease to susceptibles; and Removed, R, who are former infectives that either recovered from the disease and became immune to it (permanently or in the time frame of the analysis) or died because of the disease. It is usually assumed that no members of the Removed class are initially present. Given the timescale of a typical epidemic, birth, death (by other causes) and other demographic processes can usually be neglected. It is further assumed that the latency period is negligible, implying that an individual, once infected, immediately becomes infective. The model also assumes a perfect mixing of Susceptibles and Infectives, as a result of free motion (extensive interconnectedness) within the closed system. With these assumptions, the model can be written as the following pair of evolution steps:
The first step accounts for the infection process that occurs via close contact of an infective with a susceptible, and  is the infection rate constant. It reflects the intrinsic frequency of contacts and the probability of transmission upon contact: according to the theory of diffusion-influenced collisional processes, it can be written as  = pc, where c is the encounter rate for full diffusion control and p is the probability of transmission upon encounter [6] . The second step describes the immunization or death of infectives that thus become members of the Removed class, and  is the removal rate constant, representing the probability of transition I → R per unit time.
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The nonlinear system of differential equations corresponding to the SIR mechanism is [1] :
where S, I and R are population densities (number of class elements per unit area). As R does not appear in the first two equations, the problem is effectively reduced to a system of two (autonomous) differential equations. The dynamics is determined by four parameters: (i) Initial number of susceptibles S0; (ii) Initial number of infectives I0
(assumed to be suddenly mixed with the susceptibles at time zero). I0 is usually much smaller than S0 (it can be as low as a single individual in the entire system); (iii) Rate constant  that reflects the likeliness of disease transmission upon contact between an infective and a susceptible; (iv) Rate constant  that reflects the average time needed for an infective to be removed. The inverse of  is the average infectious period  [2] [3] [4] [5] , which is also the average duration of an infective. Another quantity of interest is the
which is the number of new infectives per unit time, as follows from equation (4).
The purpose of this work is to obtain new explicit relations for the SIR model (formulated in terms of dimensionless variables) both exact and approximate, including simple analytic solutions for the time-dependence that are valid for any R0. The paper is organized as follows: In Section 2, the SIR model is formulated in terms of dimensionless variables and the susceptibles population is explicitly related to the infectives population using both the Lambert W function and an approximate yet accurate function (sum of exponentials). The maximum value of the epidemic curve is also explicitly obtained. In Section 3, the explicit time dependence of the susceptibles, eq. (38), and infectives, eq.
(41), as well as that of the epidemic curve, eq. (45), are obtained in terms of approximate 5 analytic functions whose respective parameters are obtained in Section 4 as a function of R0. The introduced functions also allow to define analytically the respective maximum times. In Section 5, the effect of i0 (i0 << 1) on the time-dependence is shown to amount to a time shift. Finally, in Section 6 the main results are summarized.
Upon application of Laplace transforms, it follows from equations (3) and (4) that
( ) 
where  stands for the convolution between two functions. The epidemic curve thus acts as the impulse function that defines the infectives time evolution.
The system of differential equations can be rewritten in terms of five reduced (dimensionless) quantities:
where R0 is the basic reproduction number of the infection [2] [3] [4] [5] [6] . This quintet is preferable to another set, not entirely dimensionless, previously proposed [7].
Equations (3)-(5) become:
6 ( )
(16)
The initial values of s and i are 1 and i0, respectively. Usually, i0 << 1.
The reduced epidemic curve, c, is
In this way, the evolution of the system is fully defined by a single initial condition, i0, and by a single dynamic parameter, R0. This parameter has the meaning of the average number of susceptibles infected by a single infective at the beginning of the epidemic [2] [3] [4] [5] [6] [7] . Values up to 15 are known [8] , while for COVID-19 in pre-pandemic conditions it was between 2.4 and 2.5 [9, 10] . The R0 value reflects not only the intrinsic aspects of the disease, but also the population specific conditions (frequency of contacts, probability of transmission).
The threshold (or critical) number of susceptibles, is
If R0 < 1 (sc > 1), the number of infectives monotonically decreases with time (cf. equation (15) ) and the epidemic cannot proceed ('herd immunity' situation) [1] [2] [3] [4] [5] [6] . On the other hand, if R0 > 1 (sc < 1), the epidemic ensues, with the number of infectives increasing until sc is reached.
Owing to the nonlinear terms, no explicit analytical solution exists for the system of differential equations (14)-(16), and the time evolution must be obtained numerically or using approximate equations. A few analytical results are nevertheless possible.
Elimination of time from equations (14) and (15) yields
7 whose integration gives the (phase space) relation between i and s [1] [2] [3] [4] [5] [6] :
depicted in Fig. 1 . 
It is useful to solve equation (20) explicitly for s. The result is (see Appendix A):
where W0(x) is the Lambert function computed for the principal branch [11] and W-1(x) is the Lambert function computed for the secondary branch [11] . Using equations (22) 
as previously obtained from the final size equation [12, 13] . Assuming that i0 << 1, as is usually the case, equation (24) becomes ( )
For R0 higher but very close to 1, equation (25) reduces to 2/R0-1. For large R0, it becomes exp(-R0). Instead of equation (24), a simple and accurate formula (average relative error < 1% if i0 < 10 -3 ) and with the correct asymptoptic behaviour can be used,
The dependence of s on R0 is plotted in Figure 2 (see also Figure 1 ). As discussed above, there is no epidemic for R0 < 1 and the number of susceptibles does not decrease significantly (i0 << 1). The fraction of the population that does not catch the disease is about 40% for R0 = 1.5, 20% for R0 = 2, and 6% for R0 = 3. For R0 > 5 virtually the whole (initially susceptible) population is infected. Fig. 2 The fraction of susceptibles not catching the disease, s vs. the basic reproduction number R0, as given by equations (25) and (26). It is assumed that i0 << 1. Also shown is the critical value sc, equation (18) (dashed line).
Another important parameter that can be obtained is the maximum value of the epidemic curve, c* (Appendix B):
where s* stands for the number of susceptibles when the production of new infectives is at the maximum, 'epidemic peak' (Appendix B),
where W-1(x) is the Lambert W function computed for the secondary branch. For large R0
10 Finally, the areas under both i and c curves can be obtained from equations (16) and (14), respectively, and are found to be nearly identical (i0 << 1):
In this way, for large R0 (R0 > 5, say) and very small i0, both i and c curves are area normalised. The respective peak values, equations (21) and (29), respectively, agree with the fact that for large R0 the curve i() attains a stable shape (exponential decay function), with a peak value of 1+ i0, whereas the curve c() is increasingly narrow and approaches a delta function.
Obtention of simple closed-form solutions for the time-dependence of the quantities s, i, r and c has thus far eluded all efforts, unless R0 is very close to 1 [1] [2] [3] . Recently, Barlow and Weinstein [14] presented an accurate closed-form solution using asymptotic approximants. However, the number of terms needed can be quite large and no explicit relations can be obtained for characteristic quantities such as the maximum times.
A different approach is presented here, starting from the limiting results that correspond to R0 → . In fact, for large R0, one has R0 s >> 1 until s is very close to 0. In this way, virtually all S is transformed into I before R starts to form. Equation (15) can therefore be approximated by
implying that i + s = i0 + s0 in this time range. The solution of the system of equations (14) and (31) (33)
The respective i() is given by the logistic equation [15] , 
with the value ( )
compare equation (29). Equation (36) shows the effect of the initial fraction of infectives on the dynamics. The lower their number, the higher the induction time. 
where parameters a and b should reduce to 1/i0 and to (1+ i0) R0, respectively, in the limit of large R0. The parameter s is given by equation (24). The only modification in the mathematical form is thus to allow for s > 0. A simple functional form is kept, allowing to analytically compute integrals and characteristic parameters such as those for the maxima of s and c. All these quantities can indeed be obtained in closed form from the trial function equation (38). Equation (15) gives
and therefore ( ) 
Note that the alternative computation of i() from equation (14) is not effective, as a and b are no longer independent and the smoothing effect on deviations by means of integration is nonexistent.
The epidemic curve is obtained from equations (1), (17) and (38),
and the time at which the maximum ('epidemic peak') is attained is
hence the respective peak value is
compare equations (29), (36) and (37). In practice, c() is best computed using the defining equation (17).
Finally, the r curve can in principle be computed either using equation (8) 
This last relation, obtained by the elimination of time from equations (14) and (16) [3] , is less convenient as it amplifies the error of s when this quantity is close to zero.
Curve fitting for the determination of parameters a and b (fixed i0 and R0) can be performed in two ways. In the first method, the s and i curves are obtained by numerical integration, and the fitting is carried out in the time domain in a global way (i.e., minimizing a single sum of squares of deviations and using the same parameters for both curves). In the second method, fitting is carried out in the phase space, no numerical integration being necessary. In this case the exact i(s) curve is given by equation (20), and the fitting i(s) curve is given by equation (41) 
with an additional parameter (p), gives very good fits for s(), almost eliminating the somewhat too fast decay observed after the middle point, see e.g. Figures 10 and 11 . The chosen set of equations represents a compromise between accuracy and simplicity, allowing to obtain explicit expressions for the peak values and respective times, for instance equations (44), (46) and (47). as expressed by equation (7). In particular, after c() (essentially) ceases, i() decays exponentially.
The numerical results presented in the previous section refer to i0 = 0. 
Maclaurin series expansion of s gives
and therefore, for  << 1/(R0 i0), one may use s() = s(0) = 1, and equation (52) becomes
where the new initial value, '
Comparison of eq. (54) with eq. (51), rewritten as
22 gives '( ) ( )
and therefore, the time shift relations are obeyed both by s and i, 
The SIR epidemic model was formulated in terms of dimensionless variables and parameters, thus reducing the number parameters from four (S0, I0, , ) to two (i0, R0).
The susceptibles population was explicitly related to the infectives population using the Lambert W function (both the principal and the secondary branches), eqs. (22) This function is plotted in Figure A1 for R0 = 3 and i0 = 0.1. It is seen that the secondary branch, W-1(x), applies for t  [0, tmax] and the principal branch W0(x) for t  [tmax, +[. 
where W-1(x) is the Lambert W function computed for the secondary branch (see Appendix A).
The dependence of s* with R0 (i0 << 1) is plotted in Figure B1 . The reduced parameter starts from s* = 1 for R0 = 1, but quickly approaches the asymptotic value 1/2 as R0 increases and is reasonably constant for R0 > 5.
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