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A possible mechanism of susceptibility to superinfection with simian-human immunodeficiency virus (SHIV)-1157ipd3N4 was explored in twelve SHIV_SF162P3-infected Chinese rhesus macaques. Based on the kinetics of viral replication for the second infecting virus following SHIV-1157ipd3N4 inoculation, the monkeys were divided into two groups: those relatively resistant to superinfection (SIR) and those relatively sensitive to superinfection (SIS). We found that superinfection-resistant macaques had high primary viremia, whereas superinfection-sensitive macaques had low primary viremia, suggesting that primary SHIV_SF162P3 infection with a high viral-replication level would repress superinfection with a heterologous SHIV-1157ipd3N4. Although no correlation of protection against superinfection with virus-specific CD4⁺ T cell or CD8⁺ T cell immune responses from gut was observed prior to superinfection, superinfection susceptibility was strongly correlated with CD4⁺ Tcm cells from gut both prior to the second infecting virus inoculation and on day 7 after superinfection, but not with CD4⁺ Tem cells from gut or with CD4⁺ Tcm cells from peripheral blood and lymph node. These results point to the important roles of gut-derived CD4⁺ Tcm cells for the study of the mechanisms of protection against superinfection and the evaluation of the safety and efficacy of vaccines and therapies against acquired immune deficiency syndrome (AIDS).