The classical pathway or the lectin pathway can both activate the complement system (left) resulting in a proteolytic split of C3, which releases C3a and C3b. C3b (not shown) becomes a part of an enzyme known as the C5 convertase, which cleaves another complement protein called C5, releasing C5a and C5b. C5b (not shown) participates in the assembly of the membrane attack complex (MAC), which can lead to nerve damage when it forms on neuronal membranes (right). Complement cleavage products C3a and C5a can bind to the C3a receptor (C3aR) and the C5a receptor (C5aR) on myeloid cells called macrophages (top center), potentially inducing the synthesis of neuronal growth factors (NGF). NGF production could cause nerve damage through the overactivation of TRPV1 on sensory neurons. T helper cells (CD4 T cells, top left) coordinate with C3 to damage nerve cells upon HSV-1 infection. This coordination may happen through T helper cells producing interferon, which then induces myeloid cells (top center) to synthesize local complement proteins.