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Antibodies and infected monocytes and macrophages in COVID-19 patients

  • The SARS-CoV-2 virus causes the COVID-19 disease associated with over 6.2 million deaths globally. Multiple early indicators raised the potential risk of the SARS-CoV-2 virus infecting monocytes and macrophages via Fc-receptor antibody binding based on closely related beta coronaviruses. Antibody Fc-receptor infection of phagocytic monocytes and macrophages is one type of antibody dependent enhancement of disease. Increased COVID-19 severity correlated with early high antibody responses on initial infection for unvaccinated adults. Clinical evidence suggests that for moderate antibody titer levels, antibodies binding to SARS-CoV-2 may contribute to viral spread, cytokine dysregulation, and enhanced COVID-19 disease severity. Primary immune responses appear to have too low of antibody titer to significantly contribute to Fc-receptor uptake by monocytes and macrophages for COVID-19 patients. Very high antibody titers created by SARS-CoV-2 vaccines also appear to inhibit Fc-receptor uptake and infection of monocytes and macrophages; this inhibition appears to decrease as antibody titer levels decrease. Cross reactive antibodies to other coronaviruses or moderate levels of SARS-CoV-2 antibodies may be contributing to antibody dependent enhancement of disease in critical COVID-19 patients.

    Citation: Darrell O. Ricke. Antibodies and infected monocytes and macrophages in COVID-19 patients[J]. AIMS Allergy and Immunology, 2022, 6(2): 64-70. doi: 10.3934/Allergy.2022007

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  • The SARS-CoV-2 virus causes the COVID-19 disease associated with over 6.2 million deaths globally. Multiple early indicators raised the potential risk of the SARS-CoV-2 virus infecting monocytes and macrophages via Fc-receptor antibody binding based on closely related beta coronaviruses. Antibody Fc-receptor infection of phagocytic monocytes and macrophages is one type of antibody dependent enhancement of disease. Increased COVID-19 severity correlated with early high antibody responses on initial infection for unvaccinated adults. Clinical evidence suggests that for moderate antibody titer levels, antibodies binding to SARS-CoV-2 may contribute to viral spread, cytokine dysregulation, and enhanced COVID-19 disease severity. Primary immune responses appear to have too low of antibody titer to significantly contribute to Fc-receptor uptake by monocytes and macrophages for COVID-19 patients. Very high antibody titers created by SARS-CoV-2 vaccines also appear to inhibit Fc-receptor uptake and infection of monocytes and macrophages; this inhibition appears to decrease as antibody titer levels decrease. Cross reactive antibodies to other coronaviruses or moderate levels of SARS-CoV-2 antibodies may be contributing to antibody dependent enhancement of disease in critical COVID-19 patients.



    With the continuous expansion of the scale of the data center networks (DCNs), the number of servers in the network increases exponentially [1]. The server plays an important role in DCNs, which not only is used to process data but is also needed to forward data. In addition, the probability of server nodes fault is very high and the server failures cause data loss and abnormal data forwarding. Therefore, servers fault diagnosis becomes an inevitable measure to ensure a DCN reliable communication [2].

    Preparata et al. [3] proposed the first system-level fault diagnosis model, namely, the PMC model, which was used to solve the problem of automatic fault diagnosis of the multiprocessor system. Every node in the system is capable of performing tests on its adjacent node. The PMC model assumes that the tests performed by fault-free nodes are always correct, whereas tests performed by faulty nodes are unreliable. Generally, a PMC model is divided into two steps. First, adjacent nodes in the system produce test results by testing each other, which is called syndrome. Second, syndrome be analyzed to find out the faulty nodes. Typically, PMC models focus on diagnostic strategies for the second stage syndrome. Diagnosis strategy contains precise diagnosis [3], pessimistic diagnostics [4] and t/k diagnostics [5] etc. If all fault-free nodes are not mistaken for faulty nodes, it is called precise diagnosis [6]; if there are fault-free nodes that are mistaken for faulty nodes, it is called pessimistic diagnosis [7]. t/k diagnostics is that k fault-free nodes may be mistaken for faulty nodes, so precise and pessimistic diagnosis are special cases of t/k diagnosis [8]. Specifically, t/k diagnosis is precise diagnosis when k = 0, and t/k diagnosis is pessimistic diagnosis when k=1. Many diagnosis algorithms were proposed using precise, pessimistic or t/k diagnosis strategy [9,10].

    In the past, system-level fault diagnosis was commonly used in small multiprocessor systems. Nowadays, system-level fault diagnosis is more studied in DCNs with the development of DCNs. For example, Li et al. [11] studied the diagnosability of precise diagnosis and pessimistic diagnosis of DCelln,k and studied the t/k diagnosability in literature [12]. The conclusions are that the precise diagnosability of DCelln,k is n+k1, the pessimistic diagnosability is 2k+n2 when n2 and k2 and the t/k diagnosability is (k+1)(m1)+n when 1mn1. Huang H [13] studied the diagnosability of precise diagnosis of BCuben,k. The conclusion is that the precise diagnosability of BCuben,k is (n1)(k+1)1 when n2 and k0. However, they are unable to deal with large numbers of fault nodes in DCN due to their limited diagnosability. For example, DCell3,3 contains 24,492 servers with precise diagnosability of five, pessimistic diagnosability of seven and t/k diagnosability of nine. Obviously, there may be more than nine fault nodes in this network.

    To improve diagnosability, Heng et al. [14] proposed a probabilistic diagnosis method. Because it is unreliable for two unknown state nodes to test each other, the more times they tested, the more accurate the test results will be, and finally the states of the two nodes can be obtained. However, multiple tests can cause the low diagnostic efficiency and occupy the large network bandwidth, so it is not suitable for DCN networks with a large number of servers. Li et al. [15] proposed an algorithm with time complexity O(N) for hypercube-like networks by using the Hamiltonian hypercube network and gemini diagnosis structure, which greatly improves efficiency of the algorithm. Ye et al. [16] put forward five-round adaptive diagnosis in Hamiltonian networks, which greatly improves diagnosability.

    However, traditional algorithms based on the PMC model have two stages of system-level diagnosis. The first stage is to test each other between adjacent nodes, in which there may be fault nodes. The test results of fault nodes are uncertain, so it is impossible to get the correct status of all nodes through the syndrome, and it is necessary to apply the diagnosis strategy (precise or pessimistic diagnosis) to the syndrome in the second step to determine the fault node. If the test node is fault-free, then the status of the tested node can be obtained, so there is no need for a second step. This paper first proposes a fault-tolerant Hamiltonian cycle fault diagnosis algorithm (FHFD), which tests nodes in the order of the Hamiltonian cycle to ensure that the test nodes are fault-free and then combines with probability diagnosis methods to improve the diagnosability [17]. In order to improve testing efficiency, a hierarchical diagnosis strategy is also proposed, which recursively divides high scale structures into a large number of low scale structures based on the recursive structure characteristics of DCN. Concretely, we make three main contributions in the strategy.

    (1) Compared to traditional diagnosis strategies, the key difference is that our proposed strategy is more suitable for DCNs with multiple servers. This strategy greatly improves the diagnosability. 2(n2)nk1 and (n2)tn,k/tn,1 fault nodes can be accurately detected for BCuben,k and DCelln,k at most (when n3,k>0).

    (2) There is a misdiagnosis node in pessimistic diagnosis based on the traditional PMC model. The strategy we proposed ensures that the test node is fault-free by the fault-tolerant Hamiltonian cycle so that there is no misdiagnosis node.

    (3) A hierarchical diagnosis mechanism is further proposed to improve testing efficiency, which recursively divides high scale structures into a large number of low scale structures based on the recursive structure characteristics of DCNs.

    The rest of the paper is organized as follows. Preliminaries are introduced in Section 2 and diagnosis strategy based on DCNs is described in Section 3. Performance of the proposed algorithms are shown in Section 4. Finally, we conclude this paper in Section 5.

    In Section 2.1, we will present some notations and terminologies used in this paper. Then, in Section 2.2, we will describe the definition of DCell and BCube structures and some properties of Hamiltonian. Finally, in Section 2.3, we will introduce the PMC model and probabilistic diagnosis method for diagnosis.

    The topology of DCNs can be represented by an undirected graph G=(V(G),E(G)), in which V(G) is the set of vertices and E(G)={u,v|u,vV} represents the set of edges. Vertices and edges represent servers and communication links in DCNs, respectively. For an undirected graph G=(V(G),E(G)), |V| represents the number of servers in G. The edge between vertices vi and vj is denoted by (vi,vj). The neighbor set of a vertex x in G is defined as NG(x)={yV|(x,y)E}. LetLV, GL be denoted as a subgraph with V(GL)=VL,E(GL)={(x,y)E|x,y(VL)}. Path P(v0,vt)=(v0,v1,...,vt) is a sequence of different vertices (except v0 and vt) from v0 to vt, and any two consecutive vertices are adjacent. Below are the following definitions of the Hamiltonian concept:

    Hamiltonian Path: Given graph G, Vi,VjV, if P is a path from Vi to Vj that passes all vertices once, and only once, in G, then P is called a Hamiltonian path from Vi to Vj in G.

    Hamiltonian Cycle: Given graph G, Vi,VjV, starting from Vi, if P is a path from Vi to Vj that passes all vertices once, and only once, in G and finally returns to Vi, then P is called a Hamiltonian cycle from Vi to Vj in G.

    Hamiltonian connected: Given graph G, if there exists a Hamiltonian path between any distinct vertices in G, then the graph G is called Hamiltonian connected or G is a Hamiltonian connected graph.

    F(G) is used to represent the set of fault elements in graph G(V,E) (in this paper, only the set of fault servers), where F(G)V(G). Let f(G)=|F(G)| represent the number of fault servers, and if f(G)=0, then G has no faulty servers.

    Definition 1. Fk-fault-tolerant Hamiltonian graph: If GF(G) is a Hamiltonian graph, then G is an Fk-fault-tolerant Hamiltonian graph where Fk=f(G).

    Hamiltonian cycle is denoted by H(Vh,Eh) in graph G, while G(V,E) is an Fk-fault-tolerant Hamiltonian graph, where Vh=V, EhE, xiVh(1i|V|), then the Hamiltonian cycle path is H<xi1,xi2,...,xi|v|,xi1>, where <i1,i2,...,i|V|> is the sequence combination of [1,...,|V|].

    X(n,k) or Xn,k denotes a DCN with fault-tolerant Hamiltonian cycle and recursive structure, where k represents the hierarchy of structure, n represents the number of servers in X(n,0) and tn,k represents the number of servers in X(n,k).

    DCell and BCube structures exist fault-tolerant Hamiltonian cycle and are also recursive network structures. Next, the recursive construction rules of DCell and BCube and its Hamiltonian properties are introduced, which prepares for the diagnostic strategy proposed in this article.

    Definition 2 [18]. The recursive definition of DCelln,k is as follows:

    (1) DCelln,0 is a complete graph with n vertices.

    (2) When k1, DCelln,k is composed of (tn,k1+1)DCelln,k1. The (i+1)th DCelln,k1 is represented by DCellin,k1, where 0i<tn,k1+1.

    In DCelln,k, the address of the server is represented by akak1...a0(a0[0,n1],ap[0,tp1,n]p[1,k]). According to the coding rules of servers in literature [18], DCellin,k1 contains the address of the server, which is as follows:

    DCellin,k1={akak1...a0|i[0,(tn,k1+1)],ak=i%(tn,k1+1),a0[0,n1],ap[0,tp1,n],p[1,k1]}.  (2.1)

    Wang X [19] studied the Hamiltonian property of DCell and the conclusions are as follows:

    Theorem 1. When n2,k2, DCelln,k (except DCell2,1) is Hamiltonian connected and is a (n+k-3)-fault-tolerant Hamiltonian graph.

    Definition 3 [20]. The recursive definition of BCuben,k is as follows:

    (1) BCuben,0 is a complete graph with n vertices.

    (2) When k1, BCuben,k is composed of nBCuben,k1. The (i+1)th BCuben,k1 is represented by BCubein,k1, where 0i<n.

    In BCuben,k, the address of the server is represented by akak1...a0(a0[ap[0,n1],p[0,k]). According to the coding rules of servers in literature [20], BCubein,k1 contains the address of the server, which is as follows:

    DCubein,k1={akak1...a0|i[0,n],ak=i%n,ap[0,n],p[0,k1]}  (2.2)

    Huang et al. [21] studied the Hamiltonian connection of BCube and Wang et al. [22] studied the fault-tolerant Hamiltonian property of BCube, and their conclusions are as follows:

    Theorem 2. When n3,k0, BCuben,k is Hamiltonian connected, and when n4,k0, BCuben,k is a [(n1)(k+1)2]-fault-tolerant Hamiltonian graph.

    In undirected graph G=(V,E), for any two adjacent nodes (vi,vj), the notation σij is used to represent the result of vi test vj. σij = 0 represents test result as fault-free. On the contrary, σij = 1 represents test result as faulty.

    When vi is fault-free: If vj is fault-free, then σij=0; if vj is faulty, then σij=1.

    When vi is faulty: Whether vj is fault-free or faulty, its test result may be σij=0 or σij=1, and assume that the probability of σij=0 is p, where 0<p<1.

    All possible comparison results are shown in Table 1 for the PMC model.

    Table 1.  PMC model.
    vi vj σi,j
    Fault-free Fault-free 0
    Fault-free Faulty 1
    Faulty Fault-free o or 1
    Faulty Faulty 0 or 1

     | Show Table
    DownLoad: CSV

    In the PMC model, if the result of the test is σij = 0, from Table 1, we can get the corresponding three situations:

    1) Both vi and vj are fault-free;

    2) vi is faulty, but vj is fault-free;

    3) Both vi and vj are faulty.

    We cannot get the precise results though just one test; therefore, we test testing many times between two nodes before they are set to get their state and the probabilistic diagnosis method can be designed.

    Theorem 3. Four diagnosis results would be obtained through the responses of tests executed by each other r times by a pair of adjacent nodes vi and vj (r is large enough):

    (1) If r1σij=r1σji=0, then vi and vj are fault-free;

    (2) If r1σij=r&0<r1σji<r, then vi is fault-free and vj is faulty;

    (3) If 0<r1σij<r&r1σji=r, then vi is faulty and vj is fault-free;

    (4) If 0<r1σij<r&0<r1σji<r, then vi and vj are faulty;

    Proof:

    (1) If vi is faulty, the probability of r1σij=0 can be calculated by binomial distribution: P{X=k}=Crkpk(1p)rk=pk.

    Assuming that the probability of σij=0 is p = 0.5, test times r = 9 and P{X=k}=0.59=0.0019. Since the probability is too small, it can be considered that vi=0 and vj=0.

    (2) If vi = 1, the probability of r1σij=r can be calculated by binomial distribution: P{X=k}=Crkpk(1p)rk=(1p)r.

    Assuming that the probability of σij=0 is p = 0.5, test times r = 9 and P{X=k}=0.59=0.0019. Since the probability is too small, it can be considered that vi1 and vj=0. Since 0<r1σji<r and vi=0, according to the PMC rule, vj=1. Through the same logic, it can be proved that (3) holds.

    (4) Since 0<r1σij<r&0<r1σji<r, it means σji=0 or σji=1, and σji=0 or σji=1. According to the PMC rule, vi=1 and vj=1.

    We propose a novel fault diagnosis strategy, which tests nodes in the order of the Hamiltonian cycle to ensure that test nodes are fault-free. Specifically, the strategy consists of two parts: FHFD algorithm and hierarchical diagnosis method, which is suitable for DCNs with the following conditions:

    (1) Topology G(V,E) of Xn,k is Hamiltonian connected and an Fk-fault-tolerant hamiltonian graph, where k>0;

    (2)m>2, when n>2, k>0, Xn,k consists of mXn,k1, as shown in equation (3.1):

    Xn,k=(m1)(i=0)Xin,k1. (3.1)

    Xin,k1 is the (i+1)th Xn,k1, where 0i<m and m has different values on different network structures. Both BCube and DCell construct rules are shown as in Table 2.

    Table 2.  BCube and DCell construct rules.
    Xn,0 Xn,1 ... Xn,k
    BCube BCuben,0 nBCuben,0 ... nBCuben,k1
    2 DCell (tn,0+1)DCelln,0 ... (tn,k1+1)DCelln,k1

     | Show Table
    DownLoad: CSV

    (3) The address of the server in Xn,k is denoted by akak1...a0(ap[0,m1],p[0,k]). Through (1) and (2), we can distinguish different Xn,k1 by ak, as shown in equation (3.2):

    Xin,k1={akak1...a0|i[0,m],ak=i%m,ap[0,m1],p[0,k]}. (3.2)

    There exists a Hamiltonian cycle H(Vh,Eh) while a graph G(V,E) is Fk-fault-tolerant Hamiltonian. Let the H(Vh,Eh) path be H<xi1,xi2,...,xi|v|,xi1>. We first use probabilistic diagnosis in Theorem 3 to find a fault-free node as xi1, and the state of xi2 will be determined accurately according to the testing of xi1 to xi2. If xi2 is fault-free, the test outcome is accurate while xi2 tests xi3; Therefore, we can get the accurate outcome of xi3 testing xi4, for xi3 is fault-free. In turn, all nodes could be tested until the last node. On the other hand, if xi2 is faulty, two cases are discussed:

    Algorithm 1: FHFD step
    1 Constructing the hamiltonian cycle H(Vh,Eh) of G(V,E).
    2 Let xi1 test xi2 using the probability diagnosis method in Theorem 3; if xi1 = 0, let a = xi1; if xi1 = 1, then reselect two adjacent nodes to test using probabilistic diagnostic methods until the correct node is found.
    3 b,(a,b)Eh, let a test b; if σab=0, let a=b. Repeat step 3 until all nodes are detected; if σab=1, b corresponding fault node is record F(G) and step 4 is executed.
    4 Variable i is used to record the number of fault nodes; if iFk, the new Hamiltonian cycle H(Vhb,Eh) is constructed and step 3 is executed; if i>Fk, step 5 is executed.
    5 Set the next node of b as a, and the next node of a as b. Let a test b with the probability test method, and there are four situations: a=b=1, the faulty nodes a and b are recorded to F(G), and step 5 is repeated until all nodes are detected; a=b=0, let a=b and step 3 is executed; a=0 and b=1, the fault node b is recorded to F(G), and step 5 is repeated until all nodes are detected; a=1 and b=0, the fault node a is recorded to F(G), and let a = b, then step 3 is executed.

    Case 1: f(G)Fk

    G(V,E) is Fk-fault-tolerant Hamiltonian, and deleting Fk faulty nodes can still form a new Hamiltonian cycle. If f(G)Fk, the fault node xi2 can be deleted, then a new Hamiltonian cycle H(Vhxi2,Eh) is generated. Let xi1 continue to test xi3 following Hamiltonian cycle.

    Case 2: f(G)>Fk

    If xi2 is deleted when f(G)>Fk, the remaining nodes will not be able to construct a new Hamiltonian cycle, so let xi3 test xi4 using the probability diagnosis method. Due to the need for repeated tests between two nodes, the test efficiency is low and the network bandwidth is greatly occupied.

    As shown in Figure 1, X(V,E) is 1-fault-tolerant Hamiltonian graph, and the generated Hamiltonian circle is represented by H(Vh,Eh). Assuming p = 0.5, the number of test r = 9 and 91(Xi1,Xi2)=91(Xi2,Xi1)=0 satisfies Case 1 in Theorem 3, then Xi1 and Xi2 are fault-free. Let Xi2 test Xi3 so that Xi3 is faulty node and a new Hamiltonian cycle H(VhXi3,Eh) is constructed, as shown in Figure 2. Let Xi2 test Xi4 so that Xi4 is fault-free, and Xi4 test Xi5 so that Xi5 is faulty. Since X(V,E) is 1-fault-tolerant Hamiltonian graph, deleting two nodes cannot construct a new Hamiltonian cycle and the remaining nodes can use the probability diagnosis method to detect the fault.

    Figure 1.  Topology of H(Vh,Eh).
    Figure 2.  Topology of H(VhXi3,Eh)).

    For Fk-fault-tolerant Hamiltonian graph G(V,E), the relationship between the number of fault nodes and the number of tests in diagnosis is as follows:

    N={|v|2+rf(G)Fk|v|+(r2)[f(G)Fk+1]Fk<f(G). (3.3)

    In equation (3.3), N is the total number of tests, |v| denotes the number of servers in G(V,E), f(G) denotes the number of fault nodes and r is the number of times that two nodes in the probability diagnosis method need to test each other.

    BCube4,4 is 13-fault-tolerant Hamiltonian graph by Theorem 2, where Fk = 13. |v| is the number of servers, where |v| = 1024. Supposing n = 15, the numbers of tests required for different number of faulty nodes are shown in Figure 3 from equation (3.3). DCell5,2 is 4-fault-tolerant Hamiltonian graph by Theorem 1, where Fk = 4 and |v| = 930. Supposing n = 15, the numbers of tests required for different numbers of faulty nodes are shown in Figure 4 from equation (3.3).

    Figure 3.  The number of BCube4,4.
    Figure 4.  The number of BCell5,2.

    As shown in Figure 3 and Figure 4, when f(G)>Fk, the number of tests increases substantially with the number of faulty nodes. On the basis of the previous analysis, we can get that it will take up a lot of bandwidth and more time to test faulty nodes while f(G)>Fk, and when the FHFD algorithms are applied to the node diagnosis of DCNs, there will be some problems as follows because of the large scale of its servers. First, a lot of time would be spent to build Hamiltonian cycles and fault tolerant Hamiltonian cycles. Second, the nodes should be tested in the order of Hamiltonian cycles, and a complete test for the DCNs with thousands of servers will also take a lot of time.

    The total diagnostic time of the FHFD algorithm includes two parts. One part is the test time between nodes. The other part is the time consumed by constructing Hamiltonian cycles and fault-tolerant Hamiltonian cycles. We use MATLAB to simulate the FHFD algorithm for different scale networks, and the running times of the algorithm are shown in Figure 5 and Figure 6.

    Figure 5.  The test time of different scale small network.
    Figure 6.  The test time of different scale big network.

    The experimental results show that:

    1) In Figure 5, when the number of network nodes is small, the test time between nodes is greater than the time used to construct the Hamiltonian cycle. With the increase in the number of nodes, the test time between nodes does not increase much and all the time for constructing Hamiltonian cycles increases sharply.

    2) In Figure 6, when the nodes in the network reach a certain scale, the construction of Hamiltonian cycles consumes a lot of time. For example, it takes 3,000 to construct Hamiltonian cycles for the network with 196 nodes.

    The FHFD algorithm in the test process by breadth-first search to construct the fault-tolerant Hamiltonian cycle is an non-deterministic polynomial (NP)-complete problem, so when the number of nodes increases to a certain value, the time of constructing the Hamiltonian cycle increases sharply. Obviously, such a long diagnosis time cannot meet the actual situation. In the next section, we propose a hierarchical diagnosis method to solve the above problems.

    By equation (3), we have that Xn,k can be divided into mXn,k1. Each Xn,k1 can be divided into mXn,k2, and the lowest can be divided into Xn,0. Therefore, there is the following conclusion:

    Xn,k can be divided into MXn,bs (0b<k), where M is a constant (different structures have different M values):

    We consider the following two cases according to b.

    Case 1: 0<b<k

    Xn,k can be divided into MXn,bs (0<b<k) and Xn,b is an Fk-fault-tolerant Hamiltonian graph. If MXn,b are simultaneously tested, then Xn,k equals to having M Fk-fault-tolerant values. The network structure of BCube3,2 is shown in Figure 7, which can be divided into 3 BCube3,1 for simultaneous testing. By equation (4), Xin,k1={akak1...a0|i[0,m],ak=i%m}; therefore, the nodes contained in BCube3,2 can be divided:

    BCube03,1={000,001,002,010,011,012,020,021,022}
    BCube13,1={100,101,102,110,111,112,120,121,122}
    BCube23,1={200,201,202,210,211,212,220,221,222}
    Figure 7.  The test time of different scale big network.

    By theorem 2, BCube3,2 is 4-fault-tolerant Hamiltonian graph, where fault-tolerant values Fk = 4. BCube3,1 is 2-fault-tolerant Hamiltonian graph, where degree of diagnosability Fk = 2. When the FHFD algorithm is applied to BCube03,1, BCube13,1 and BCube23,1 to complete the test, the sum of fault-tolerant values of three BCube3,1 are Fk = 6, which is two more than fault-tolerant values of BCube3,2, thereby increasing the degree of diagnosability.

    BCube4,4 can be divided into MBCube4,b (0<b<k) and different values of b corresponding M and fault-tolerant values Fk are shown in Table 3.

    Table 3.  Fault-tolerant values of BCube4,4.
    M Fk MFk
    BCube4,3 4 10 40
    BCube4,2 16 7 112
    BCube4,1 64 4 256

     | Show Table
    DownLoad: CSV

    Table 3 shows that the smaller b, the greater the fault tolerance value Fk could be obtained. However, the central server needs to send and collect information to all BCube4,b at the same time during the parallel testing, and a higher performance central server is needed to increase costs with larger M. Therefore, for a more appropriate division of Xn,k into M Xn,b (0<b<k), there is the following equation (3.4):

    H=α|F|βT(tn,p)γC(M). (3.4)

    In equation (3.4), |F| represents the sum of fault-tolerant values Fk of MXn,bs and T(tn,p) represents the time spent on tn,p server tests. C(M) represents performance requirements for central servers. α,β,γ are the weights, and their values of different network structures are also different. The larger the H value, the more reasonable the division.

    For example, when α=0.1,β=0.1,γ=0.5, BCube4,4 can be divided into BCube4,3, BCube4,2 or BCube4,1. The equation (6) can get the following values by taking into the above value.

    H(BCube4,3)=0.14

    H(BCube4,2)=0.77

    H(BCube4,1)=0.76

    Since H(BCube4,2) is the largest, it is most reasonable to divide BCube4,4 into 16 BCube4,2.

    Case 2: b=0

    Xn,k is divided into MXn,0, where n is sufficiently large. By definition 2 and 3, Xn,0 is a complete graph G(V,E) and x,xV,NG(x)=Vx. That is, x is adjacent to all other nodes. If x is fault-free, using x to test the remaining nodes in Xn,0 can accurately measure the state of other nodes. This case does not need to generate a Hamiltonian cycle for diagnosis, which can greatly improve the test efficiency.

    In this section, the FHFD algorithm and hierarchical testing method are applied to BCube and DCell networks, respectively, and their diagnosabilities are analyzed and compared with traditional diagnostic strategies.

    The diagnosability of the FHFD algorithm (in only Case 1) combined with hierarchical test method for DCell is as follows:

    Theorem 4: The maximum diagnosability of DCelln,k is (n2)(tn,k/tn,1) by combining the FHFD algorithm and hierarchical test method with n4 and k>0.

    Proof: DCelln,k can be divided into (tn,k/tn,1)DCelln,1 by equation (3) and DCelln,1 is (n-2)-fault tolerant Hamiltonian by Theorem 1, then the sum of fault tolerant value of (tn,k/tn,1)DCelln,1 is (n2)(tn,k/tn,1).

    We summarize the diagnosability of DCelln,k based on different strategies in the PMC model in Table 4, which shows that the FHFD algorithm combined with hierarchical testing can greatly improve the diagnosability.

    Table 4.  Diagnosability of DCelln,k.
    DCell3,2 DCell4,2 DCell3,3 DCell4,3
    tnk 156 420 24492 176820
    precise 4 5 5 6
    pessimistic 5 6 7 8
    t/c 6 7 9 12
    FHFD+Hierarchical 13 42 2041 17682

     | Show Table
    DownLoad: CSV

    This section will study the diagnosability of the FHFD algorithm (in only Case 1) combined with hierarchical test method for BCube.

    Theorem 5: The maximum diagnosability of BCuben,k is 2(n2)nk1 by combining the FHFD algorithm and hierarchical test method while n4 and k>0.

    Proof: By equation (3), BCuben,k=nk1BCuben,1 and BCuben,1 is 2(n-2)-fault tolerant Hamiltonian by Theorem 2 and, thus, the sum of diagnosability of nk1BCuben,1 is 2(n2)nk1.

    We summarize the diagnosability of BCuben,k based on different strategies in the PMC model in Table 5, which shows that the FHFD algorithm combined with hierarchical testing can greatly improve the degree of diagnosability.

    Table 5.  Diagnosability of BCuben,k.
    BCube3,2 BCube4,2 BCube3,3 BCube4,3
    tnk 64 256 1024 4096
    precise 8 11 14 17
    FHFD+Hierarchical 16 64 256 1024

     | Show Table
    DownLoad: CSV

    This section simulates the test time of FHFD and the hierarchical method in BCube network by MATLAB, as shown in Figure 8.

    Figure 8.  The testing time of FHFD algorithm and hierarchical method.

    (1) BCube3,4 has 243 server nodes, and diagnosis only spends 0.97s. BCube4,4 has 1,024 nodes and diagnosis only spends 5.12s, which shows that the time consumed increases linearly as the number of server nodes increases. This result proves that server nodes have a significant impact on diagnostic time.

    (2) BCube4,4 has 1,024 nodes and spends 5.12s in the actual test. BCube6,3 has 1296 nodes and spends 21.38s in the actual test, which shows that the size of the two networks is similar but the test time is quite different. The reason is that the two are divided into layers through the Hierarchical Diagnosis Based on Recursive (HDBR) algorithm. BCube6,1contains 36 nodes, BCube4,1 contains 16 nodes and the time is different to construct Hamiltonian cycles for 36 nodes and 16 nodes, resulting in a large difference in the final test time but it is still acceptable.

    In this paper, we proposed a novel node fault diagnosis strategy based on the PMC model in DCNs structure, satisfying recursiveness by using fault-tolerant Hamiltonian cycle property. Compared with the traditional diagnosis strategy, our proposed strategy can meet the characteristics of high diagnosability, high accuracy and high efficiency. Therefore, this strategy is more suitable for system-level fault diagnosis of DCNs.

    The authors declare they have not used Artificial Intelligence (AI) tools in the creation of this article.

    This work was supported by the National Natural Science Foundation of China (61672209, 61701170, 62173127, 61973104), Grain Information Processing Center in Henan University of Technology (KFJJ-2020-111), China Postdoctoral Science Foundation funded project (2014M560439), Jiangsu Planned Projects for Postdoctoral Research Funds (1302084B), Scientific & Technological Support Project of Jiangsu Province (BE2016185) and the Science and technology development plan of Henan Province (192102210282, 202102210327).

    The authors declare there is no conflict of interest.



    Conflict of interest



    The author declare no conflict of interest.

    [1] Ricke DO (2021) Two different antibody-dependent enhancement (ADE) risks for SARS-CoV-2 antibodies. Front Immunol 12: 443. https://doi.org/10.3389/fimmu.2021.640093
    [2] Jaume M, Yip MS, Cheung CY, et al. (2011) Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH-and cysteine protease-independent FcγR pathway. J Virol 85: 10582-10597. https://doi.org/10.1128/JVI.00671-11
    [3] Junqueira C, Crespo Â, Ranjbar S, et al. (2022) FcγR-mediated SARS-CoV-2 infection of monocytes activates inflammation. Nature . In press. https://doi.org/10.1038/s41586-022-04702-4
    [4] Wan Y, Shang J, Sun S, et al. (2020) Molecular mechanism for antibody-dependent enhancement of coronavirus entry. J Virol 94: e02015-19. https://doi.org/10.1128/JVI.02015-19
    [5] Lee N, Chan PKS, Ip M, et al. (2006) Anti-SARS-CoV IgG response in relation to disease severity of severe acute respiratory syndrome. J Clin Virol 35: 179-184. https://doi.org/10.1016/j.jcv.2005.07.005
    [6] Peiris J, Lai S, Poon L, et al. (2003) Coronavirus as a possible cause of severe acute respiratory syndrome. Lancet 361: 1319-1325. https://doi.org/10.1016/S0140-6736(03)13077-2
    [7] Hsueh PR, Hsiao CH, Yeh SH, et al. (2003) Microbiologic characteristics, serologic responses, and clinical manifestations in severe acute respiratory syndrome, Taiwan. Emerg Infect Dis 9: 1163-1167. https://doi.org/10.3201/eid0909.030367
    [8] Wang H, Rao S, Jiang C (2007) Molecular pathogenesis of severe acute respiratory syndrome. Microbes Infect 9: 119-126. https://doi.org/10.1016/j.micinf.2006.06.012
    [9] Pujadas E, Chaudhry F, McBride R, et al. (2020) SARS-CoV-2 viral load predicts COVID-19 mortality. Lancet Respir Med 8: e70. https://doi.org/10.1016/S2213-2600(20)30354-4
    [10] Yan X, Chen G, Jin Z, et al. (2022) Anti-SARS-CoV-2 IgG levels in relation to disease severity of COVID-19. J Med Virol 94: 380-383. https://doi.org/10.1002/jmv.27274
    [11] Luo YR, Chakraborty I, Yun C, et al. (2021) Kinetics of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antibody avidity maturation and association with disease severity. Clin Infect Dis 73: e3095-e3097. https://doi.org/10.1093/cid/ciaa1389
    [12] Fajnzylber J, Regan J, Coxen K, et al. (2020) SARS-CoV-2 viral load is associated with increased disease severity and mortality. Nat Commun 11: 5493. https://doi.org/10.1038/s41467-020-19057-5
    [13] Chen W, Zhang J, Qin X, et al. (2020) SARS-CoV-2 neutralizing antibody levels are correlated with severity of COVID-19 pneumonia. Biomed Pharmacother 130: 110629. https://doi.org/10.1016/j.biopha.2020.110629
    [14] Chen H, Qin R, Huang Z, et al. (2021) Characteristics of COVID-19 patients based on the results of nucleic acid and specific antibodies and the clinical relevance of antibody levels. Front Mol Biosci 7: 605862. https://doi.org/10.3389/fmolb.2020.605862
    [15] Young BE, Ong SWX, Ng LFP, et al. (2021) Viral dynamics and immune correlates of coronavirus disease 2019 (COVID-19) severity. Clin Infect Dis 73: e2932-e2942. https://doi.org/10.1093/cid/ciaa1280
    [16] Liu X, Wang J, Xu X, et al. (2020) Patterns of IgG and IgM antibody response in COVID-19 patients. Emerg Microbes Infect 9: 1269-1274. https://doi.org/10.1080/22221751.2020.1773324
    [17] Atyeo C, Fischinger S, Zohar T, et al. (2020) Distinct early serological signatures track with SARS-CoV-2 survival. Immunity 53: 524-532. https://doi.org/10.1016/j.immuni.2020.07.020
    [18] Fraley E, LeMaster C, Banerjee D, et al. (2021) Cross-reactive antibody immunity against SARS-CoV-2 in children and adults. Cell Mol Immunol 18: 1826-1828. https://doi.org/10.1038/s41423-021-00700-0
    [19] Shrwani K, Sharma R, Krishnan M, et al. (2021) Detection of serum cross-reactive antibodies and memory response to SARS-CoV-2 in prepandemic and post-COVID-19 convalescent samples. J Infect Dis 224: 1305-1315. https://doi.org/10.1093/infdis/jiab333
    [20] Miyara M, Saichi M, Sterlin D, et al. (2022) Pre-COVID-19 immunity to common cold human coronaviruses induces a recall-type IgG response to SARS-CoV-2 antigens without cross-neutralisation. Front Immunol 13: 790334. https://doi.org/10.3389/fimmu.2022.790334
    [21] Aguilar-Bretones M, Westerhuis BM, Raadsen MP, et al. (2021) Seasonal coronavirus-specific B cells with limited SARS-CoV-2 cross-reactivity dominate the IgG response in severe COVID-19. J Clin Invest 131: e150613. https://doi.org/10.1172/JCI150613
    [22] Cheng Y, Wong R, Soo YOY, et al. (2005) Use of convalescent plasma therapy in SARS patients in Hong Kong. Eur J Clin Microbiol 24: 44-46. https://doi.org/10.1007/s10096-004-1271-9
    [23] Korley FK, Durkalski-Mauldin V, Yeatts SD, et al. (2021) Early convalescent plasma for high-risk outpatients with Covid-19. N Engl J Med 385: 1951-1960. https://doi.org/10.1056/NEJMoa2103784
    [24] Horby PW, Landray MJ, Grp RC (2021) Convalescent plasma in patients admitted to hospital with COVID-19 (RECOVERY): a randomised controlled, open-label, platform trial. Lancet 397: 2049-2059. https://doi.org/10.1016/S0140-6736(21)00897-7
    [25] De Santis GC, Oliveira LC, Garibaldi PMM, et al. (2022) High-dose convalescent plasma for treatment of severe COVID-19. Emerg Infect Dis 28: 548-555. https://doi.org/10.3201/eid2803.212299
    [26] Axfors C, Janiaud P, Schmitt AM, et al. (2021) Association between convalescent plasma treatment and mortality in COVID-19: a collaborative systematic review and meta-analysis of randomized clinical trials. BMC Infect Dis 21: 1170. https://doi.org/10.1186/s12879-021-06829-7
    [27] García-Nicolás O, V'kovski P, Zettl F, et al. (2021) No evidence for human monocyte-derived macrophage infection and antibody-mediated enhancement of SARS-CoV-2 infection. Front Cell Infect Microbiol 11: 644574. https://doi.org/10.3389/fcimb.2021.644574
    [28] Boumaza A, Gay L, Mezouar S, et al. (2021) Monocytes and macrophages, targets of severe acute respiratory syndrome coronavirus 2: the clue for coronavirus disease 2019 immunoparalysis. J Infect Dis 224: 395-406. https://doi.org/10.1093/infdis/jiab044
    [29] Martines RB, Ritter JM, Matkovic E, et al. (2020) Pathology and pathogenesis of SARS-CoV-2 associated with fatal coronavirus disease, United States. Emerg Infect Dis 26: 2005-2015. https://doi.org/10.3201/eid2609.202095
    [30] Grant RA, Morales-Nebreda L, Markov NS, et al. (2021) Circuits between infected macrophages and T cells in SARS-CoV-2 pneumonia. Nature 590: 635-641. https://doi.org/10.1038/s41586-020-03148-w
    [31] Feng Z, Diao B, Wang R, et al. (2020) The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) directly decimates human spleens and lymph nodes. medRxiv Preprint . https://doi.org/10.1101/2020.03.27.20045427
    [32] Wang C, Xie J, Zhao L, et al. (2020) Alveolar macrophage dysfunction and cytokine storm in the pathogenesis of two severe COVID-19 patients. eBioMedicine 57: 102833. https://doi.org/10.1016/j.ebiom.2020.102833
    [33] Martínez-Colón GJ, Ratnasiri K, Chen H, et al. (2021) SARS-CoV-2 infects human adipose tissue and elicits an inflammatory response consistent with severe COVID-19. bioRxiv Preprint . https://doi.org/10.1101/2021.10.24.465626
    [34] Tavazzi G, Pellegrini C, Maurelli M, et al. (2020) Myocardial localization of coronavirus in COVID-19 cardiogenic shock. Eur J Heart Fail 22: 911-915. https://doi.org/10.1002/ejhf.1828
    [35] Yang L, Han Y, Jaffré F, et al. (2021) An immuno-cardiac model for macrophage-mediated inflammation in COVID-19 hearts. Circ Res 129: 33-46. https://doi.org/10.1161/CIRCRESAHA.121.319060
    [36] Percivalle E, Sammartino JC, Cassaniti I, et al. (2021) Macrophages and monocytes: “Trojan horses” in COVID-19. Viruses 13: 2178. https://doi.org/10.3390/v13112178
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