Assessment of the hypothetical protein BB0616 in the murine infection of Borrelia burgdorferi

Lyme disease is the most common vector-borne infection, with an estimated 476,000 new cases annually in the United States (1, 2). Clinical manifestations range from characteristic skin lesions called “erythema migrans” to carditis, arthritis, and neuroborreliosis. This disease is caused by the spirochetal pathogen Borrelia burgdorferi (also known as Borreliella burgdorferi), which is transmitted to humans through hematophagous bites of an arthropod tick vector (usually Ixodes ticks) (3–5). B. burgdorferi is maintained in nature through an infectious cycle involving ticks and mammalian hosts. The acquisition of B. burgdorferi occurs when newly hatched larvae feed on infected reservoir hosts, e.g., small rodents, during which B. burgdorferi enters the ticks together with the bloodmeal and then colonizes the tick midgut. Following colonization, spirochetes reside in this nutritionally limited environment through the molt into the nymphal stage. When nymphs attach to and take a bloodmeal on the subsequent hosts, spirochetes traverse the tick midgut peritrophic membrane, migrate through the hemocoel to the salivary gland, and then are deposited into the host skin to initiate infection. Once in the host, B. burgdorferi disseminates hematogenously into distant organs and causes tissue damage.