CD8+ T cell mediated noncytolytic inhibition of human immunodeficiency virus type I

Abstract

The development of cellular immune responses in primary human immunodeficiency virus type-1 (HIV-1) infection is accompanied by a dramatic decrease in plasma viremia and resolution of the acute clinical syndrome. The full nature of the immunological response and its consequences on HIV pathogenesis is still largely a mystery, but significant progress has been achieved in the characterization of some of the players involved. Several studies indicate that noncytolytic HIV suppression by CD8+ T lymphocytes may be inversely associated with viral load suggesting that this antiviral activity is important in host control of HIV replication. This review focuses on this antiviral activity by CD8+ T lymphocytes, which is distinct from that activity elicited by some cytolytic CD8+ T lymphocytes (CTLs).

A Soluble Factor(s) Secreted from CD8+T Lymphocytes Inhibits Human Immunodeficiency Virus Type 1 Replication through STAT1 Activation

“…One component of this response is the secretion of an antiviral factor(s) from CD8 ϩ T cells (50,87). This may not be a specific response to HIV-1 but is perhaps a more general reflection of how the immune system responds to viral pathogens.…”

Amino-Terminal Fragment of Urokinase-Type Plasminogen Activator Inhibits HIV-1 Replication

“…ϩ T lymphocytes have the activity that suppresses HIV-1 replication in the absence of cell killing and the inhibitory effect could be mediated by the soluble factors (1)(2)(3). Some soluble factors have been reported to have the HIV-1 suppressive activities with various mechanisms.…”

Initial HIV-1 Antigen-Specific CD8 + T Cells in Acute HIV-1 Infection Inhibit Transmitted/Founder Virus Replication

“…Furthermore, the characterization of the cytokine profile of CD8 ϩ T cells has identified MIP-1␤ as a correlate of virus control (16) and virus inhibition (18). In total, CD8 ϩ T cells can inhibit virus replication through either lysis of infected CD4 ϩ T cells or inhibition of virus replication (7,13,41,54,55,59). This inhibition may involve suppression through the release of soluble ␤-chemokines that can directly block the entry of CCR5-using viruses (8,14).…”