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Research article

Reaction-diffusion model of HIV infection of two target cells under optimal control strategy

  • † These authors contributed equally to the work
  • In order to study the effects of reverse transcriptase inhibitors, protease inhibitors and flavonoids on two target cells infected by HIV in a heterogeneous environment, an HIV mathematical model at the cellular level was established. Research shows that infected cells can be categorized into immature infected cells, latent infected cells, and mature infected cells based on the infection process. The basic reproduction number R0 was established, and it is proved that R0 serves as a threshold parameter: When R0<1, the disease-free steady state is globally asymptotically stable, and the disease is extinct; when R0>1, the solution of the system is uniformly persistent, and the virus exists. Considering the huge advantages of drug intervention in controlling HIV infection, the optimal control problem was proposed under the condition that the constant diffusion coefficient is positive, so as to minimize the total number of HIV-infected cells and the cost of drug treatment. To illustrate our theoretical results, we performed numerical simulations in which the model parameters were obtained with reference to some medical studies. The results showed that: (1) as R0 increases, the risk of HIV transmission increases; (2) pharmacological interventions are important in early treatment of HIV spread and control of viral load in the body; (3) the treatment process must consider the heterogeneity of medication, otherwise it will not be conducive to suppressing the spread of the virus and will increase costs.

    Citation: Ziang Chen, Chunguang Dai, Lei Shi, Gaofang Chen, Peng Wu, Liping Wang. Reaction-diffusion model of HIV infection of two target cells under optimal control strategy[J]. Electronic Research Archive, 2024, 32(6): 4129-4163. doi: 10.3934/era.2024186

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  • In order to study the effects of reverse transcriptase inhibitors, protease inhibitors and flavonoids on two target cells infected by HIV in a heterogeneous environment, an HIV mathematical model at the cellular level was established. Research shows that infected cells can be categorized into immature infected cells, latent infected cells, and mature infected cells based on the infection process. The basic reproduction number R0 was established, and it is proved that R0 serves as a threshold parameter: When R0<1, the disease-free steady state is globally asymptotically stable, and the disease is extinct; when R0>1, the solution of the system is uniformly persistent, and the virus exists. Considering the huge advantages of drug intervention in controlling HIV infection, the optimal control problem was proposed under the condition that the constant diffusion coefficient is positive, so as to minimize the total number of HIV-infected cells and the cost of drug treatment. To illustrate our theoretical results, we performed numerical simulations in which the model parameters were obtained with reference to some medical studies. The results showed that: (1) as R0 increases, the risk of HIV transmission increases; (2) pharmacological interventions are important in early treatment of HIV spread and control of viral load in the body; (3) the treatment process must consider the heterogeneity of medication, otherwise it will not be conducive to suppressing the spread of the virus and will increase costs.


    A semiring is an algebra with two associative binary operations +,, in which + is commutative and distributive over + from the left and right. Such an algebra is a common generalization of both rings and distributive lattices. It has broad applications in information science and theoretical computer science (see [5,6]). In this paper, we shall investigate some small-order semirings which will play a crucial role in subsequent follows.

    The semiring A with addition and multiplication table (see [12])

    +0a10000a0a010010a10000a01a10a1

    The semiring B with addition and multiplication table (see [4])

    +abcaabcbbbbccbcabcaaaabbbbcabc

    Eight 2-element semirings with addition and multiplication table (see [2])

    Semiring + Semiring +
    L2 0 1
    1 1
    0 0
    1 1
    R2 0 1
    1 1
    0 1
    0 1
    M2 0 1
    1 1
    0 1
    1 1
    D2 0 1
    1 1
    0 0
    0 1
    N2 0 1
    1 1
    0 0
    0 0
    T2 0 1
    1 1
    1 1
    1 1
    Z2 0 0
    0 0
    0 0
    0 0
    W2 0 0
    0 0
    0 0
    0 1

     | Show Table
    DownLoad: CSV

    For any semiring S, we denote by S0 the semiring obtained from S by adding an extra element 0 and where a=0+a=a+0,0=0a=a0 for every aS. For any semiring S, S will denote the (multiplicative) left-right dual of S. In 2005, Pastijn et al. [4,9,10] studied the semiring variety generated by B0 and (B0) (Denoted by Sr(2,1)). They showed that the lattice of subvarieties of this variety is distributive and contains 78 varieties precisely. Moreover, each of these is finitely based. In 2016, Ren et al. [12,13] studied the variety generated by B0,(B0) and A0 (Denoted by Sr(3,1)). They showed that the lattice of subvarieties of this variety is distributive and contains 179 varieties precisely. Moreover, each of these is finitely based. From [4,10], we have HSP(L2,R2,M2,D2)HSP(B0,(B0)). So

    HSP(L2,R2,M2,D2)HSP(L2,R2,M2,D2,Z2,W2)HSP(B0,(B0),Z2,W2).

    In 2016, Shao and Ren [15] studied the variety HSP(L2,R2,M2,D2,Z2,W2) (Denoted by S6). They showed that the lattice of subvarieties of this variety is distributive and contains 64 varieties precisely. Moreover, each of these is finitely based. Recently, Ren and Zeng [14] studied the variety generated by B0,(B0),N2,T2. They proved that the lattice of subvarieties of this variety is a distributive lattice of order 312 and that each of its subvarieties is finitely based. In [16], Wang, Wang and Li studied the variety generated by B0,(B0),A0,N2,T2. They proved that the lattice of subvarieties of this variety is a distributive lattice of order 716 and that each of its subvarieties is finitely based. It is easy to check

    HSP(B0,(B0),A0,N2,T2)HSP(B0,(B0),A0,N2,T2,Z2,W2).

    So semiring variety HSP(B0,(B0),A0,N2,T2) is a proper subvariety of the semiring variety HSP(B0,(B0),A0,N2,T2,Z2,W2). The main purpose of this paper is to study the variety HSP(B0,(B0), A0,N2,T2,Z2,W2). We show that the lattice of subvarieties of this variety is a distributive lattice of order 2327. Moreover, we show this variety is hereditarily finitely based.

    By a variety we mean a class of algebras of the same type that is closed under subalgebras, homomorphic images and direct products (see [11]). Let W be a variety, let L(W) denote the lattice of subvarieties of W and let IdW(X) denote the set of all identities defining W. If W can be defined by finitely many identities, then we say that W is finitely based (see [14]). In other words, W is said to be finitely based if there exists a finite subset Σ of IdW(X) such that for any pqIdW(X), pq can be derived from Σ, i.e., Σpq. Otherwise, we say that W is nonfinitely based. Recall that W is said to be hereditarily finitely based if all members of L(W) are finitely based. If a variety W is finitely based and L(W) is a finite lattice, then W is hereditarily finitely based (see [14]).

    A semiring is called an additively idempotent semiring (ai-semiring for short) if its additive reduct is a semilattice, i.e., a commutative idempotent semigroup. It is also called a semilattice-ordered semigroup (see [3,8,12]). The variety of all semirings (resp. all ai-semirings) is denoted by SR (resp. AI). Let X denote a fixed countably infinite set of variables and X+ the free semigroup on X (see [8]). A semiring identity (SR-identity for short) is an expression of the form uv, where u and v are terms with u=u1++uk, v=v1++v, where ui,vjX+. Let k_ denote the set {1,2,,k} for a positive integer k, Σ be a set of identities which include the identities determining AI (Each identity in Σ is called an AI-identity) and uv be an AI-identity. It is easy to check that the ai-semiring variety defined by uv coincides with the ai-semiring variety defined by the identities uu+vj,vv+ui,ik_,j_. Thus, in order to show that uv is derivable from Σ, we only need to show that uu+vj,vv+ui,ik_,j_ can be derived from Σ (see [9]).

    To solve the word problem for the variety HSP(B0,(B0),A0,N2,T2,Z2,W2), the following notions and notations are needed. Let q be an element of X+. Then

    ● the head of q, denoted by h(q), is the first variable occurring in q;

    ● the tail of q, denoted by t(q), is the last variable occurring in q;

    ● the content of q, denoted by c(q), is the set of variables occurring in q;

    ● the length of q, denoted by |q|, is the number of variables occurring in q counting multiplicities;

    ● the initial part of q, denoted by i(q), is the word obtained from q by retaining only the first occurrence of each variable;

    ● the final part of q, denoted by f(q), is the word obtained from q by retaining only the last occurrence of each variable;

    r(q) denotes set {xX|the number of occurrences of x in q is odd}.

    By [13,Lemma 1.2], Sr(3,1) satisfies the identity pq if and only if (i(p),f(p),r(p))=(i(q),f(q), r(q)). This result will be used later without any further notice. The basis for each one of N2,T2,Z2,W2 can be found from [2] (See Table 1).

    Table 1.  Bases for N2,T2,Z2,W2.
    Semiring Equational basis Semiring Equational basis
    N2 xyzt,x+x2x T2 xyzt,x+x2x2
    Z2 x+yz+u,xyx+y W2 x+yz+u,x2x,xyyx

     | Show Table
    DownLoad: CSV

    By [15,Lemma 1.1] and the Table 1, we have

    Lemma 2.1. Let uv be a nontrivial SR-identity, where u=u1+u2++um, v=v1+v2++vn, ui,vjX+, im_,jn_. Then

    (i) N2uvifandonlyif{uiu||ui|=1}={viv||vi|=1};

    (ii) T2uvifandonlyif{uiu||ui|2}ϕ,{viv||vi|2}ϕ;

    (iii) Z2uvifandonlyif(xX)ux,vx;

    (iv) W2uvifandonlyifm=n=1,c(u1)=c(v1)orm,n2.

    Suppose that u=u1++um,uiX+,im_. Let 1 be a symbol which is not in X and Y an arbitrary subset of i=mi=1c(u1). For any ui in u, if c(ui)Y, put hY(ui)=1. Otherwise, we shall denote by hY(ui) the first variable occurring in the word obtained from ui by deleting all variables in Y. The set {hY(ui)|uiu} is written HY(u). Dually, we have the notations tY(ui) and TY(ui). In particular, if Y=, then hY(ui)=h(ui) and tY(ui)=t(ui). Moreover, if c(ui)Y for every ui in u, then we write DY(u)=. Otherwise, DY(u) is the sum of all terms ui in u such that c(ui)Y=. By [13,Lemma 2.3 and 2.11] and [4,Lemma 2.4 and its dual,Lemma 2.5 and 2.6], we have

    Lemma 2.2. Let uu+q be an AI-identity, where u=u1++um,ui,qX+,im_. If uu+q holds in Sr(3,1), then

    (i) for every Zi=mi=1c(ui)c(q), there exists p1 in X+ with r(p1)=r(q) and c(q)c(p1)i=ki=1c(ui) such that DZ(u)DZ(u)+p1 holds in Sr(3,1), where DZ(u)=u1++uk.

    (ii) for every YZ=i=mi=1c(ui)c(q), HY(DZ(u))=HY(DZ(u)+p1) and TY(DZ(u))=TY(DZ(u)+p1).

    Throughout this paper, u(3.1),(3.2),v denotes the identity uv can be derived from the identities (3.1),(3.2), and the identities determining SR. For other notations and terminology used in this paper, the reader is referred to [1,4,7,13,15].

    In this section, we shall show that the variety HSP(B0,(B0),A0,N2,T2,Z2,W2) is finitely based. Indeed, we have

    Theorem 3.1. The semiring variety HSP(B0,(B0),A0,N2,T2,Z2,W2) is determined by (3.1)–(3.12),

    x3yxy; (3.1)
    xy3xy; (3.2)
    (xy)2x2y2; (3.3)
    (xy)3xy; (3.4)
    x2yxxyx2; (3.5)
    xyzxxyx2zx; (3.6)
    xy+zxy+z+xyz2; (3.7)
    xy+zxy+z+z2xy; (3.8)
    xy+zxy+z+xz2y; (3.9)
    xy+zxy+z+z3; (3.10)
    x+y+ztx+y+zt+xzty; (3.11)
    x+yx+y+y. (3.12)

    Proof. From [13] and Lemma 2.1, we know that both Sr(3,1) and HSP(N2,T2,Z2,W2) satisfy identities (3.1)–(3.12) and so does HSP(B0,(B0),A0,N2,T2,Z2,W2).

    Next, we shall show that every identity that holds in HSP(B0,(B0),A0,N2,T2,Z2,W2) can be derived from (3.1)–(3.12) and the identities determining SR. Let uv be such an identity, where u=u1+u2++um, v=v1+v2++vn, ui,vjX+, 1im,1jn. By Lemma 2.1 (ⅳ), we only need to consider the following two cases:

    Case 1. m=n=1 and c(u1)=c(v1). From Sr(3,1),T2,Z2u1v1, it follows that (i(u1),f(u1),r(u1))=(i(v1),f(v1),r(v1)), |u1|2 and |v1|2. Hence u1(3.1)(3.6)v1.

    Case 2. m,n2. It is easy to verify that uv and the identity (3.12) imply the identities uu+vj, vv+ui for all i,j such that 1im,1jn. Conversely, the latter m+n identities imply uu+vv. Thus, to show that uv is derivable from (3.1)–(3.12) and the identities determining SR, we need only show that the simpler identities uu+vj, vv+ui for all i,j such that 1im,1jn. Hence we need to consider the following two cases:

    Case 2.1. uu+q, where |q|=1. Since N2uu+q, there exists us=q. Thus u+qu+us+qu+us+us(3.12)u+usu.

    Case 2.2. uu+q, where |q|2. Since uu+q holds in T2, it follows from Lemma 2.1 (ⅱ) that there exists ui in u such that ui>1. Put Z=(i=mi=1c(ui))c(q). Assume that DZ(u)=u1++uk. Then i=ki=1c(ui)=c(q). By Lemma 2.2 (ⅰ), there exists p1X+ such that r(p1)=r(q) and c(q)c(p1)i=ki=1c(ui). Moreover,

    uu+ui+DZ(u)u+ui+p1+DZ(u)u+ui+p1+DZ(u)+p31(by (3.10))u+ui+p1+DZ(u)+p31+p31u21u22u2k.(by (3.7))

    Write p=p31u21u22u2k. Thus c(p)=c(q), r(p)=r(q) and we have derived the identity

    uu+p. (3.13)

    Due to |p|>1, it follows that (3.4) implies the identity

    p3p. (3.14)

    Suppose that i(q)=x1x2x. We shall show by induction on j that for every 1j, uu+x21x22x2p is derivable from (3.1)–(3.11) and the identities defining SR.

    From Lemma 2.1 (ⅱ), there exists ui1 in DZ(u) with c(ui1)c(q) such that h(ui1)=h(q)=x1. Furthermore,

    uu+ui1+p(by (3.13))u+ui1+p+u2i1p(by (3.8))u+ui1+p+x21u2i1p(by (3.1))u+ui1+p+x21u2i1p+x21p2u2iip(by (3.9))u+ui1+p+x21u2i1p+x21p.(by (3.6), (3.14))

    Therefore

    uu+x21p. (3.15)

    Assume that for some 1<j,

    uu+x21x22x2j1p (3.16)

    is derivable from (3.1–3.12) and the identities defining SR. By Lemma 2.1 (ⅱ), there exists ui in DZ(u) with c(ui)c(q) such that ui=ui1xjui2 and c(ui1){x1,x2,,xj1}. It follows that

    uu+ui+pu+ui+p+u2ip(by (3.8))u+ui+p+u2i1x2ju2i2p(by (3.3))u+ui+p+u2i1x2ju2i2p+u2i1x2jp2u2i2p(by (3.9))u+ui+p+u2i1x2ju2i2p+u2i1x2jp.(by (3.6), (3.14))

    Consequently

    uu+u2i1x2jp. (3.17)

    Moreover, we have

    uu+x21x22x2j1p+u2i1x2jp(by (3.16), (3.17))u+x21x22x2j1p+u2i1x2jp+x21x22x2j1(u2i1x2jp)2p(by (3.9))u+x21x22x2j1p+u2i1x2jp+x21x22x2j1x2jp.(by (3.3), (3.6), (3.14)))

    Hence uu+x21x22x2j1x2jp. Using induction we have

    uu+i2(q)p. (3.18)

    Dually,

    uu+pf2(q). (3.19)

    Thus

    uu+p+i2(q)p+pf2(q)(by (3.13), (3.18), (3.19))u+p+i2(q)p+pf2(q)+i2(q)pppf2(q)(by (3.11))u+p+i2(q)p+pf2(q)+i2(q)pf2(q)(by (3.14))u+p+i2(q)p+pf2(q)+q.(by (3.1)–(3.6))

    It follows that uu+q.

    In this section we characterize the lattice L(HSP(B0,(B0),A0,N2,T2,Z2,W2)). Throughout this section, t(x1,,xn) denotes the term t which contains no other variables than x1,,xn (but not necessarily all of them). Let SHSP(B0,(B0),A0,N2,T2,Z2,W2) and let E+(S) denote the set {aS|a+a=a}, where any element of E+(S) is said to be an additive idempotent of (S,+). Notice that HSP(B0,(B0),A0,N2,T2,Z2,W2) satisfies the identities

    (x+y)+(x+y)(x+x)+(y+y), (4.1)
    xy+xy(x+x)(y+y). (4.2)

    By (4.1) and (4.2), it is easy to verify that E+(S)={a+a|aS} forms a subsemiring of S. To characterize the lattice L(HSP(B0,(B0),A0,N2,T2,Z2,W2)), we need to consider the following mapping

    φ:L(HSP(B0,(B0),A0,N2,T2,Z2,W2))L(HSP(B0,(B0),A0,N2,T2)),WWHSP(B0,(B0),A0,N2,T2). (4.3)

    It is easy to prove that φ(W)={E+(S)|SW} for each member W of L(HSP(B0,(B0),A0,N2,T2, Z2,W2)). If W is the subvariety of HSP(B0,(B0),A0,N2,T2) determined by the identities

    ui(xi1,,xin)vi(xi1,,xin),ik_,

    then ˆW denotes the subvariety of HSP(B0,(B0),A0,N2,T2,Z2,W2) determined by the identities

    ui(xi1+xi1,,xin+xin)vi(xi1+xi1,,xin+xin),ik_. (4.4)

    Lemma 4.1. [16] The ai-semiring variety HSP(B0,(B0),A0,N2,T2) is determined by the identities (3.1)–(3.11) and L(HSP(B0,(B0),A0,N2,T2)) is a distributive lattice of order 716.

    Lemma 4.2. Let W be a member of L(HSP(B0,(B0),A0,N2,T2)). Then, ˆW=WHSP(Z2,W2).

    Proof. Since W satisfies the identities (4.4), it follows that W is a subvariety of ˆW. Both Z2 and W2 are members of ˆW and so WHSP(Z2,W2)ˆW. To show the converse inclusion, it suffices to show that every identity that is satisfied by WHSP(Z2,W2) can be derived by the identities holding in HSP(B0,(B0),A0,N2,T2,Z2,W2) and

    ui(xi1+xi1,,xin+xin)vi(xi1+xi1,,xin+xin),ik_,

    if W is the subvariety of L(HSP(B0,(B0),A0,N2,T2)) determined by ui(xi1,,xin)vi(xi1,,xin), ik_. Let uv be such an identity, where u=u1+u2++um,v=v1+v2++vn,ui,vjX+,1im,1jn. By Lemma 2.1 (8), we only need to consider the following two cases.

    Case 1. m,n2. By identity (3.12), HSP(B0,(B0),A0,N2,T2,Z2,W2) satisfies the identities

    u+uu, (4.5)
    v+vv. (4.6)

    Since uv holds in HSP(B0,(B0),A0,N2,T2), we have that it is derivable from the collection Σ of uivi,ik_ and the identities determining HSP(B0,(B0),A0,N2,T2). From [1,Exercise Ⅱ.14.11], it follows that there exist t1,t2,,tPf(X+) such that

    t1=u,t=v;

    ● For any i=1,2,,1, there exist pi,qi,riPf(X+) (where pi, qi and ri may be empty words), a semiring substitution φi and an identity uiviΣ such that

    ti=piφi(wi)qi+ri,ti+1=piφi(si)qi+ri,where eitherwi=ui,si=viorwi=vi,si=ui.

    Let Σ denote the set {u+uv+v|uvΣ}. For any i=1,2,,1, we shall show that ti+titi+1+ti+1 is derivable from Σ and the identities holding in HSP(B0,(B0),A0,N2,T2,Z2,W2). Indeed, we have

    ti+ti=piφi(wi)qi+ri+piφi(wi)qi+ripiφi(wi)qi+piφi(wi)qi+ri+ripi(φi(wi+wi))qi+ri+ripi(φi(si+si))qi+ri+ri(sincewi+wisi+siΣorsi+siwi+wiΣ)piφi(si)qi+piφi(si)qi+ri+ripiφi(si)qi+ri+piφi(si)qi+ri=ti+1+ti+1.

    Further,

    u+u=t1+t1t2+t2t+t=v+v.

    This implies the identity

    u+uv+v. (4.7)

    We now have

    u(4.6)u+u(4.7)v+v(4.6)v. (4.8)

    Case 2. m=n=1 and c(u)=c(v). Since Z2u1v1, u1x,v1x, for every xX. Since u1v1 holds in HSP(B0,(B0),A0,N2,T2), we have that it is derivable from the collection Σ of uivi,ik_ and the identities defining HSP(B0,(B0),A0,N2,T2). From [1,Exercise Ⅱ.14.11], it follows that there exist t1,t2,,tPf(X+) such that

    t1=u1,t=v1;

    ● For any i=1,2,,1, there exist pi,qiPf(X+) (where pi and qi may be empty words), a semiring substitution φi and an identity uiviΣ (where ui and vi are words) such that

    ti=piφi(wi)qi,ti+1=piφi(si)qi,where eitherwi=ui,si=viorwi=vi,si=ui.

    By Lemma 4.1, we have that u1v1 can be derived from (3.1)–(3.6), so, by Theorem 3.1, it can be derived from monomial identities holding in HSP(B0,(B0),A0,N2,T2,Z2,W2). This completes the proof.

    Lemma 4.3. The following equality holds

    L(HSP(B0,(B0),A0,N2,T2,Z2,W2))=WL(HSP(B0,(B0),A0,N2,T2))[W,ˆW]. (4.9)

    There are 716 intervals in L(HSP(B0,(B0),A0,N2,T2,Z2,W2)), and each interval is a congruence class of the kernel of the complete epimorphism φ in (4.3).

    Proof. Firstly, we shall show that equality (4.9) holds. It is easy to see that

    L(HSP(B0,(B0),A0,N2,T2,Z2,W2))=WL(HSP(B0,(B0),A0,N2,T2))φ1(W).

    So it suffices to show that

    φ1(W)=[W,ˆW], (4.10)

    for each member W of L(HSP(B0,(B0),A0,N2,T2)). If W1 is a member of [W,ˆW], then it is routine to verify that W{E+(S)|SW1}W. This implies that {E+(S)|SW1}=W and so φ(W1)=W. Hence, W1 is a member of φ1(W) and so [W,ˆW]φ1(W). Conversely, if W1 is a member of φ1(W), then W=φ(W1)={E+(S)|SW1} and so φ1(W)[W,ˆW]. This shows that (4.9) holds.

    From Lemma 4.1, we know that L(HSP(B0,(B0),A0,N2,T2)) is a lattice of order 716. So there are 716 intervals in L(HSP(B0,(B0),A0,N2,T2,Z2,W2)). Next, we show that φ a complete epimorphism. On one hand, it is easy to see that φ is a complete -epimorphism. On the other hand, let (Wi)iI be a family of members of L(HSP(B0,(B0),A0,N2,T2,Z2, W2)). Then, by (4.3), we have that φ(Wi)Wi^φ(Wi) for each iI. Further,

    iIφ(Wi)iIWiiI^φ(Wi)^iIφ(Wi).

    This implies that φ(iIWi)=iIφ(Wi). Thus, φ is a complete -homomorphism and so φ is a complete -epimorphism. By (4.10), we deduce that each interval in (4.3) is a congruence class of the kernel of the complete epimorphism φ.

    In order to characterize the lattice L(HSP(B0,(B0),A0,N2,T2,Z2,W2)), by Lemma 4.3, we only need to describe the interval [W,ˆW] for each member W of L(HSP(B0, (B0),A0,N2,T2)). Next, we have

    Lemma 4.4. Let W be a member of L(HSP(B0,(B0),A0,N2,T2)). Then, WHSP(Z2) is the subvariety of ˆW determined by the identity

    x3x3+x3. (4.11)

    Proof. It is easy to see that both, W and HSP(Z2) satisfy the identity (4.11) and so does WHSP(Z2). In the following we prove that every identity that is satisfied by WHSP(Z2) is derivable from (4.11) and the identities holding in ˆW. Let uv be such an identity, where u=u1+u2++um,v=v1+v2++vn,ui,vjX+,1im,1jn. We only need to consider the following cases.

    Case 1. m=n=1. Since Z2 satisfies u1v1, it follows that |u1|1 and |v1|1. By Lemma 4.2, ˆW satisfies the identity u31+u31v31+v31. Hence u1(3.4)u31(4.11)u31+u31v31+v31(4.11)v31(3.4)v1.

    Case 2. m=1, n2. Since Z2 satisfies u1v, it follows that |u1|1. By Lemma 4.2, ˆW satisfies the identity u31+u31v+v. Hence u1(3.4)u31(4.11)u31+u31v+v(3.11)v.

    Case 3. m2, n=1. Similar to Case 2.

    Case 4. m,n2. By Lemma 4.2, ˆW satisfies the identity u+uv+v. Hence u(3.11)u+uv+v(3.11)v.

    Lemma 4.5. Let W be a member of L(Sr(3,1)). Then WHSP(W2) is the subvariety of ˆW determined by the identities

    x3x. (4.12)

    Proof. It is easy to see that both, W and HSP(W2) satisfy the identity (4.12) and so does WHSP(W2). So it suffices to show that every identity that is satisfied by WHSP(W2) is derivable from (4.12) and the identities holding in ˆW. Let uv be such an identity, where u=u1+u2++um,v=v1+v2++vn,ui,vjX+,1im,1jn. By Lemma 4.2, ˆW satisfies the identity u3v3. Hence, u(4.12)u3v3(4.12)v.

    Lemma 4.6. Let W be a member of L(HSP(B0,(B0),A0,N2,T2)). Then the interval [W,ˆW] of L(HSP(B0,(B0),A0,N2,T2,Z2,W2)) is given in Figure 1.

    Figure 1.  The interval [W,ˆW].

    Proof. Suppose that W1 is a member of [W,ˆW] such that W1ˆW and W1W. Then, there exists a nontrivial identity uv holding in W1 such that it is not satisfied by ˆW. Also, we have that W1 does not satisfy the identity x+xx. By Lemma 4.2, we only need to consider the following two cases.

    Case 1. HSP(Z2)uv,HSP(W2)uv. Then, uv satisfies one of the following three cases:

    m=n=1, c(u1)c(v1), |u1|1 and |v1|1;

    m=1,n>1 and |u1|1;

    m>1,n=1 and |v1|1.

    It is easy to see that, in each of the above cases, uv can imply the identity x3x3+x3. By Lemma 4.4, we have that W1 is a subvariety of WHSP(Z2). On the other hand, since W1x3x3+x3 and W1x+xx, it follows that Z2 is a member of W1 and so WHSP(Z2) is a subvariety of W1. Thus, W1=WHSP(Z2).

    Case 2. HSP(Z2)uv,HSP(W2)uv. Then, uv satisfies one of the following two cases:

    m=n=1, c(u1)=c(v1) and |u1|=1;

    m=n=1, c(u1)=c(v1) and |v1|=1.

    If N2,T2W, then, in each of the above cases, uv can imply the identity xx3. By Lemma 4.5, W1 is a subvariety of WHSP(W2). On the other hand, since W1xx3 and W1xx+x, it follows that W2 is a member of W1 and so WHSP(W2) is a subvariety of W1. Thus, W1=WHSP(W2).

    If N2W, then, by Lemma 2.1 (ⅰ), |u1|=|v1|=1, a contradiction. Thus, V1=ˆV.

    If T2W, then, by Lemma 2.1 (ⅱ), |u1|2,|v1|2, a contradiction. Thus, V1=ˆV.

    By Lemma 4.3 and 4.6, we can show that the lattice L(HSP(B0,(B0),A0,N2,T2,Z2, W2)) of subvarieties of the variety HSP(B0,(B0),A0,N2,T2,Z2,W2) contains 2327 elements. In fact, we have

    Theorem 4.7. L(HSP(B0,(B0),A0,N2,T2,Z2,W2)) is a distributive lattice of order 2327.

    Proof. We recall from [16] that Sr(3,1)T2 [Sr(3,1)N2] contains 358 subvarieties since Sr(3,1) contains 179 subvarieties. By Lemma 4.3 and 4.6, we can show that L(HSP(B0,(B0),A0,N2,T2,Z2, W2)) has exactly 2327 (where 2327=179×4+358×3×2179×3) elements. Suppose that W1,W2 and W3 are members of L(HSP(B0,(B0),A0, N2,T2,Z2,W2)) such that W1W2=W1W3 and W1W2=W1W3. Then, by Lemma 4.3

    φ(W1)φ(W2)=φ(W1)φ(W3)

    and

    φ(W1)φ(W2)=φ(W1)φ(W3).

    Since L(HSP(B0,(B0),A0,N2,T2) is distributive, it follows that φ(W2)=φ(W3). Write W for φ(W2). Then both W2,W3 are members of [W,ˆW]. Suppose that W2W3. Then, by Lemma 4.6, W1W2=W1W3 and W1W2=W1W3 can not hold at the same time. This implies that W2=W3.

    By Theorem 4.1, 4.7 and [14,Corollary 1.2], we now immediately deduce

    Corollary 4.8. HSP(B0,(B0),A0,N2,T2,Z2,W2) is hereditarily finitely based.

    This article considers a semiring variety generated by B0,(B0),A0,N2,T2,Z2,W2. The finite basis problem for semirings is an interesting developing topic, with plenty of evidence of a high level of complexity along the lines of the more well-developed area of semigroup varieties. This article is primarily a contribution toward the property of being hereditarily finite based, meaning that all subvarieties are finitely based. This property is of course useful because it guarantees the finite basis property of a large number of examples.

    This work was supported by the Natural Science Foundation of Chongqing (cstc2019jcyj-msxmX0156, cstc2020jcyj-msxmX0272, cstc2021jcyj-msxmX0436), the Scientific and Technological Research Program of Chongqing Municipal Education Commission (KJQN202001107, KJQN202101130) and the Scientific Research Starting Foundation of Chongqing University of Technology (2019ZD68).

    The authors declare that they do not have any conflict of interests regarding this paper.



    [1] X. Tian, J. Chen, X. Wang, Y. Xie, X. Zhang, D. Han, et al., Global, regional, and national HIV/AIDS disease burden levels and trends in 1990–2019: A systematic analysis for the global burden of disease 2019 study, Front. Public Health, 11 (2023), 1068664. https://doi.org/10.3389/fpubh.2023.1068664 doi: 10.3389/fpubh.2023.1068664
    [2] D. Jahagirdar, M. K. Walters, A. Novotney, E. D. Brewer, T. D. Frank, A. Carter, et al., Global, regional, and national sex-specific burden and control of the HIV epidemic, 1990–2019, for 204 countries and territories: the Global Burden of Diseases Study 2019, Lancet HIV, 8 (2021), e633–e651. https://doi.org/10.1016/S2352-3018(21)00152-1 doi: 10.1016/S2352-3018(21)00152-1
    [3] S. K. Cribbs, K. Crothers, A. Morris, Pathogenesis of HIV-related lung disease: Immunity, infection, and inflammation, Physiol. Rev., 100 (2020), 603–632. https://doi.org/10.1152/physrev.00039.2018 doi: 10.1152/physrev.00039.2018
    [4] A. S. Fauci, G. Pantaleo, S. Stanley, D. Weissman, Immunopathogenic mechanisms of HIV infection, Ann. Int. Med., 124 (1996), 654–663. https://doi.org/10.7326/0003-4819-124-7-199604010-00006 doi: 10.7326/0003-4819-124-7-199604010-00006
    [5] R. F. Siliciano, W. C. Greene, HIV latency, Cold Spring Harbor Perspect. Med., 1 (2011), a007096. https://doi.org/10.1101/cshperspect.a007096 doi: 10.1101/cshperspect.a007096
    [6] N. H. Alshamrani, Stability of a general adaptive immunity HIV infection model with silent infected cell-to-cell spread, Chaos Solitons Fractals, 150 (2021), 110422. https://doi.org/10.1016/j.chaos.2020.110422 doi: 10.1016/j.chaos.2020.110422
    [7] Y. Yang, R. Xu, Mathematical analysis of a delayed HIV infection model with saturated CTL immune response and immune impairment, J. Appl. Math. Comput., 68 (2022), 2365–2380. https://doi.org/10.1007/s12190-021-01621-x doi: 10.1007/s12190-021-01621-x
    [8] Y. Tian, X. Liu, Global dynamics of a virus dynamical model with general incidence rate and cure rate, Nonlinear Anal. Real World Appl., 16 (2014), 17–26. https://doi.org/10.1016/j.nonrwa.2013.09.002 doi: 10.1016/j.nonrwa.2013.09.002
    [9] A. Korobeinikov, Global properties of basic virus dynamics models, Bull. Math. Biol., 66 (2004), 879–883. https://doi.org/10.1016/j.bulm.2004.02.001 doi: 10.1016/j.bulm.2004.02.001
    [10] X. Wang, Q. Ge, Y. Chen, Threshold dynamics of an HIV infection model with two distinct cell subsets, Appl. Math. Lett., 103 (2020), 106242. https://doi.org/10.1016/j.aml.2020.106242 doi: 10.1016/j.aml.2020.106242
    [11] P. W. Nelson, A. S. Perelson, Mathematical analysis of delay differential equation models of HIV-1 infection, Math. Biosci., 179 (2002), 73–94. https://doi.org/10.1016/S0025-5564(02)00099-8 doi: 10.1016/S0025-5564(02)00099-8
    [12] W. Zuo, M. Shao, Stationary distribution, extinction and density function for a stochastic HIV model with a Hill-type infection rate and distributed delay, Electron. Res. Arch., 30 (2022), 4066–4085. https://doi.org/10.3934/era.2022206 doi: 10.3934/era.2022206
    [13] R. Zhang, J. Wang, On the global attractivity for a reaction–diffusion malaria model with incubation period in the vector population, J. Math. Biol., 84 (2022), 53. https://doi.org/10.1007/s00285-022-01751-1 doi: 10.1007/s00285-022-01751-1
    [14] M. Cao, J. Zhao, J. Wang, R. Zhang, Dynamical analysis of a reaction-diffusion vector-borne disease model incorporating age-space structure and multiple transmission routes, Commun. Nonlinear. Sci., 127 (2023), 107550. https://doi.org/10.1016/j.cnsns.2023.107550 doi: 10.1016/j.cnsns.2023.107550
    [15] A. S. Perelson, D. E. Kirschner, R. De Boer, Dynamics of HIV infection of CD4+ T cells, Math. Biosci., 114 (1993), 81–125. https://doi.org/10.1016/0025-5564(93)90043-A doi: 10.1016/0025-5564(93)90043-A
    [16] V. Müller, J. F. Vigueras-Gómez, S. Bonhoeffer, Decelerating decay of latently infected cells during prolonged therapy for human immunodeficiency virus type 1 infection, J. Virol., 76 (2002), 8963–8965. https://doi.org/10.1128/jvi.76.17.8963-8965.2002 doi: 10.1128/jvi.76.17.8963-8965.2002
    [17] H. Wang, R. Xu, Z. Wang, H. Chen, Global dynamics of a class of HIV-1 infection models with latently infected cells, Nonlinear Anal. Model., 20 (2015), 21–37. https://doi.org/10.15388/NA.2015.1.2 doi: 10.15388/NA.2015.1.2
    [18] X. Wang, J. Yang, X. Luo, Asymptotical profiles of a viral infection model with multi-target cells and spatial diffusion, Comput. Math. Appl., 77 (2019), 389–406. https://doi.org/10.1016/j.camwa.2018.09.043 doi: 10.1016/j.camwa.2018.09.043
    [19] K. Wang, W. Wang, Propagation of HBV with spatial dependence, Math. Biosci., 210 (2007), 78–95. https://doi.org/10.1016/j.mbs.2007.05.004 doi: 10.1016/j.mbs.2007.05.004
    [20] D. S. Green, D. M. Center, W. W. Cruikshank, Human immunodeficiency virus type 1 gp120 reprogramming of CD4+ T-cell migration provides a mechanism for lymphadenopathy, J. Virol., 83 (2009), 5765–5772. https://doi.org/10.1128/jvi.00130-09 doi: 10.1128/jvi.00130-09
    [21] H. Ewers, V. Jacobsen, E. Klotzsch, A. E. Smith, A. Helenius, V. Sandoghdar, Label-free optical detection and tracking of single virions bound to their receptors in supported membrane bilayers, Nano Lett., 7 (2007), 2263–2266. https://doi.org/10.1021/nl070766y doi: 10.1021/nl070766y
    [22] H. Boukari, B. Brichacek, P. Stratton, S. F. Mahoney, J. D. Lifson, L. Margolis, et.al., Movements of HIV-virions in human cervical mucus, Biomacromolecules, 10 (2009), 2482–2488. https://doi.org/10.1021/bm900344q doi: 10.1021/bm900344q
    [23] M. C. Strain, D. D. Richman, J. K. Wong, H. Levine, Spatiotemporal dynamics of HIV propagation, J. Theoret. Biol., 218 (2002), 85–96. https://doi.org/10.1006/jtbi.2002.3055 doi: 10.1006/jtbi.2002.3055
    [24] P. Wu, H. Zhao, Dynamical analysis of a nonlocal delayed and diffusive HIV latent infection model with spatial heterogeneity, J. Franklin Inst., 358 (2021), 5552–5587. https://doi.org/10.1016/j.jfranklin.2021.05.014 doi: 10.1016/j.jfranklin.2021.05.014
    [25] F. B. Wang, Y. Huang, X. Zou, Global dynamics of a PDE in-host viral model, Appl. Anal., 93 (2014), 2312–2329. https://doi.org/10.1080/00036811.2014.955797 doi: 10.1080/00036811.2014.955797
    [26] D. Baleanu, M. Hasanabadi, A. M. Vaziri, A. Jajarmi, A new intervention strategy for an HIV/AIDS transmission by a general fractional modeling and an optimal control approach, Chaos Solitons Fractals, 167 (2023), 113078. https://doi.org/10.1016/j.chaos.2022.113078 doi: 10.1016/j.chaos.2022.113078
    [27] E. F. Arruda, C. M. Dias, C. V. de Magalhã, D. H. Pastore, R. C. Thomé, H. M. Yang, An optimal control approach to HIV immunology, Appl. Math., 6 (2015), 1115–1130. https://doi.org/10.4236/am.2015.66102 doi: 10.4236/am.2015.66102
    [28] K. O. Okosun, O. D. Makinde, I. Takaidza, Impact of optimal control on the treatment of HIV/AIDS and screening of unaware infectives, Appl. Math. Model., 37 (2013), 3802–3820. https://doi.org/10.1016/j.apm.2012.08.004 doi: 10.1016/j.apm.2012.08.004
    [29] T. T. Yusuf, F. Benyah, Optimal strategy for controlling the spread of HIV/AIDS disease: A case study of South Africa, J. Biol. Dyn., 6 (2012), 475–494. https://doi.org/10.1080/17513758.2011.628700 doi: 10.1080/17513758.2011.628700
    [30] A. L. Hill, D. I. Rosenbloom, M. A. Nowak, R. F. Siliciano, Insight into treatment of HIV infection from viral dynamics models, Immunol. Rev., 285 (2018), 9–25. https://doi.org/10.1111/imr.12698 doi: 10.1111/imr.12698
    [31] M. Markowitz, M. Louie, A. Hurley, E. Sun, M. Di Mascio, A. S. Perelson, et al., A novel antiviral intervention results in more accurate assessment of human immunodeficiency virus type 1 replication dynamics and T-cell decay in vivo, J. Virol., 77 (2003), 5037–5038. https://doi.org/10.1128/jvi.77.8.5037-5038.2003 doi: 10.1128/jvi.77.8.5037-5038.2003
    [32] A. Andrade, S. L. Rosenkranz, A. R. Cillo, D. Lu, E. S. Daar, J. M. Jacobson, et al., Three distinct phases of HIV-1 RNA decay in treatment-naive patients receiving raltegravir-based antiretroviral therapy: ACTG A5248, J. Infect. Dis., 208 (2013), 884–891. https://doi.org/10.1093/infdis/jit272 doi: 10.1093/infdis/jit272
    [33] E. F. Cardozo, A. Andrade, J. W. Mellors, D. R. Kuritzkes, A. S. Perelson, R. M. Ribeiro, Treatment with integrase inhibitor suggests a new interpretation of HIV RNA decay curves that reveals a subset of cells with slow integration, PLoS Pathog., 13 (2017), e1006478. https://doi.org/10.1371/journal.ppat.1006478 doi: 10.1371/journal.ppat.1006478
    [34] Y. Lou, X. Q. Zhao, A reaction-diffusion malaria model with incubation period in the vector population, J. Math. Biol., 62 (2011), 543–568. https://doi.org/10.1007/s00285-010-0346-8 doi: 10.1007/s00285-010-0346-8
    [35] H. L. Smith, Monotone Dynamical Systems: An Introduction to the Theory of Competitive and Cooperative Systems, American Mathematical Soc., 1995.
    [36] R. H. Martin, H. L. Smith, Abstract functional-differential equations and reaction-diffusion systems, Am. Math. Soc., 321 (1990), 1–44. https://doi.org/10.2307/2001590 doi: 10.2307/2001590
    [37] R. B. Guenther, J. W. Lee, Partial Differential Equations of Mathematical Physics and Integral Equations, Dover Publications Inc., Mineola, 1996.
    [38] M. Wang, Nonlinear Elliptic Equations, Science Public.
    [39] J. Wu, Theory and Applications of Partial Functional Differential Equations, Springer Science & Business Media, New York, 2012.
    [40] J. K. Hale, Asymptotic Behavior of Dissipative Systems, American Mathematical Soc., Providence, 2010.
    [41] W. Wang, X. Q. Zhao, Basic reproduction numbers for reaction-diffusion epidemic models, SIAM J. Appl. Dyn. Syst., 11 (2012), 1652–1673. https://doi.org/10.1137/120872942 doi: 10.1137/120872942
    [42] H. R. Thieme, Convergence results and a Poincaré-Bendixson trichotomy for asymptotically autonomous differential equations, J. Math. Biol., 30 (1992), 755–763. https://doi.org/10.1007/bf00173267 doi: 10.1007/bf00173267
    [43] H. Smith, X. Q. Zhao, Robust persistence for semidynamical systems, Nonlinear Anal. Theor., 47 (2001), 6169–6179. https://doi.org/10.1016/s0362-546x(01)00678-2 doi: 10.1016/s0362-546x(01)00678-2
    [44] P. Magal, X. Q. Zhao, Global attractors and steady states for uniformly persistent dynamical systems, SIAM J. Math. Anal., 37 (2005), 251–275. https://doi.org/10.1137/S0036141003439173 doi: 10.1137/S0036141003439173
    [45] D. Kirschner, S. Lenhart, S. Serbin, Optimal control of the chemotherapy of HIV, J. Math. Biol., 35 (1997), 775–792. https://doi.org/10.1007/s002850050076 doi: 10.1007/s002850050076
    [46] M. Zhou, H. Xiang, Z. Li, Optimal control strategies for a reaction-diffusion epidemic system, Nonlinear Anal. Real World Appl., 46 (2019), 446–464. https://doi.org/10.1016/j.nonrwa.2018.09.023 doi: 10.1016/j.nonrwa.2018.09.023
    [47] J. P. Raymond, F. Tröltzsch, Second Order Sufficient Optimality Conditions For Nonlinear Parabolic Control Problems With State Constraints, Techn. Univ. Chemnitz, Fakultät Für Mathematik, 1998.
    [48] S. Zheng, Nonlinear Evolution Equations, Chapman and Hall/CRC, 2004.
    [49] J. L. Lions, Optimal Control of Systems Governed by Partial Differential Equations, Springer, Berlin, 1971.
    [50] S. Nakaoka, S. Iwami, K. Sato, Dynamics of HIV infection in lymphoid tissue network, J. Math. Biol., 72 (2016), 909–938. https://doi.org/10.1007/s00285-015-0940-x doi: 10.1007/s00285-015-0940-x
    [51] G. A. Funk, V. A. Jansen, S. Bonhoeffer, T. Killingback, Spatial models of virus-immune dynamics, J. Theor. Biol., 233 (2005), 221–236. https://doi.org/10.1016/j.jtbi.2004.10.004 doi: 10.1016/j.jtbi.2004.10.004
    [52] P. W. Nelson, J. D. Murray, A. S. Perelson, A model of HIV-1 pathogenesis that includes an intracellular delay, Math. Biosci., 163 (2000), 201–215. https://doi.org/10.1016/S0025-5564(99)00055-3 doi: 10.1016/S0025-5564(99)00055-3
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